炎癥、癲癇發作和癲癇發生：對人類疾病的探索_Journal of Epilepsy

Authors：

 TanTH , PeruccaP , O'BrienTJ , 高凡凱　李碩　譯 , 薛國芳　審

Corresponding?author：

TanTH, Email: mastura.monif@monash.edu

Keywords：

神經系統自身免疫性疾病、細胞因子、癲癇、癲癇發作

DOI：

10.7507/2096-0247.202204010

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癲癇在歷史上被認為是一種神經元信號異常傳導的疾病，表現為癲癇發作。隨著大量自身抗體的發現和對自身免疫性腦炎認識的不斷加深，人們越來越重視先天性和適應性免疫系統在癲癇發作和癲癇發生中的作用。在不同的癲癇發作相關的神經炎癥和自身免疫疾病中，不同程度觀察到了致病性抗體、補體激活、CD8⁺細胞毒性T細胞和小膠質細胞激活。這些異常的免疫反應被認為會導致神經元信號傳導破壞，產生急性癥狀性癲癇發作，并且在某些情況下，還會發展為長期的自身免疫性癲癇。雖然早期使用免疫調節療法可以改善自身免疫性腦炎和自身免疫性癲癇的預后，但患者的識別和治療方法的選擇并不總是明確。本篇綜述討論了免疫系統的不同成分在各種形式的癲癇發作中的作用，包括自身免疫性腦炎、自身免疫性癲癇、Rasmussen腦炎、熱性感染相關性癲癇綜合征和新發難治性癲癇持續狀態。尤其是討論了在這些疾病中觀察到的病理生理學和獨特的細胞因子譜，及其與診斷、預后和治療決策的聯系。

Citation： TanTH, PeruccaP, O'BrienTJ, 高凡凱　李碩　譯, 薛國芳　審. 炎癥、癲癇發作和癲癇發生：對人類疾病的探索. Journal of Epilepsy, 2022, 8(4): 348-365. doi: 10.7507/2096-0247.202204010 Copy

1.	Wandinger KP, Leypoldt F, Junker R. Autoantibody-Mediated Encephalitis. Dtsch Arztebl Int, 2018, 115(40): 666-673.
2.	Spatola M, Dalmau J. Seizures and risk of epilepsy in autoimmune and other inflammatory encephalitis. Curr Opin Neurol, 2017, 30(3): 345-353.
3.	Nabbout R, Vezzani A, Dulac O, et al. Acute encephalopathy with inflammation-mediated status epilepticus. Lancet Neurol, 2011, 10(1): 99-108.
4.	Gaspard N, Foreman BP, Alvarez V, et al. New-onset refractory status epilepticus: Etiology, clinical features, and outcome. Neurology, 2015, 85(18): 1604-1613.
5.	Kramer U, Chi CS, Lin KL, et al. Febrile infection-related epilepsy syndrome (FIRES): pathogenesis, treatment, and outcome: a multicenter study on 77 children. Epilepsia, 2011, 52(11): 1956-1965.
6.	Vezzani A, Balosso S, Ravizza T. Neuroinflammatory pathways as treatment targets and biomarkers in epilepsy. Nat Rev Neurol, 2019, 15(8): 459-472.
7.	Vezzani A, Dingledine R, Rossetti AO. Immunity and inflammation in status epilepticus and its sequelae: possibilities for therapeutic application. Expert review of neurotherapeutics, 2015, 15(9): 1081-1092.
8.	van Vliet EA, Aronica E, Vezzani A, et al. Neuroinflammatory pathways as treatment targets and biomarker candidates in epilepsy: emerging evidence from preclinical and clinical studies. Neuropathology and applied neurobiology, 2018, 44(1): 91-111.
9.	Holtkamp M, Othman J, Buchheim K, et al. Predictors and prognosis of refractory status epilepticus treated in a neurological intensive care unit. Journal of neurology, neurosurgery, and psychiatry, 2005, 76(4): 534-539.
10.	Santamarina E, Gonzalez M, Toledo M, et al. Prognosis of status epilepticus (SE): relationship between SE duration and subsequent development of epilepsy. Epilepsy & Behavior, 2015, 49: 138-140.
11.	Hesdorffer DC, Logroscino G, Cascino G, et al. Risk of unprovoked seizure after acute symptomatic seizure: effect of status epilepticus. Annals of neurology, 1998, 44(6): 908-912.
12.	Ruiz-García R, Martínez-Hernández E, Saiz A, et al. The diagnostic value of onconeural antibodies depends on how they are tested. Frontiers in immunology, 2020, 11: 1482.
13.	Geis C, Planagumà J, Carre?o M, et al. Autoimmune seizures and epilepsy. The Journal of clinical investigation, 2019, 129(3): 926-940.
14.	Graus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol, 2016, 15(4): 391-404.
15.	Tüzün E, Dalmau J. Limbic encephalitis and variants: classification, diagnosis and treatment. The neurologist, 2007, 13(5): 261-271.
16.	Esposito S, Principi N, Calabresi P, et al. An evolving redefinition of autoimmune encephalitis. Autoimmunity reviews, 2019, 18(2): 155-163.
17.	Quek AML, O'Toole O. Autoimmune epilepsy: the evolving science of neural autoimmunity and its impact on epilepsy management. Seminars in neurology, 2018, 38(3): 290-302.
18.	Bien CG, Vincent A, Barnett MH, et al. Immunopathology of autoantibody-associated encephalitides: clues for pathogenesis. Brain: a journal of neurology, 2012, 135(Pt 5): 1622-1638.
19.	Rada A, Birnbacher R, Gobbi C, et al. Seizures associated with antibodies against cell surface antigens are acute symptomatic and not indicative of epilepsy: insights from long-term data. Journal of neurology, 2021, 268(3): 1059-1069.
20.	Steriade C, Britton J, Dale RC, et al. Acute symptomatic seizures secondary to autoimmune encephalitis and autoimmune-associated epilepsy: Conceptual definitions. Epilepsia, 2020, 61(7): 1341-1351.
21.	van Sonderen A, Thijs RD, Coenders EC, et al. Anti-LGI1 encephalitis: clinical syndrome and long-term follow-up. Neurology, 2016, 87(14): 1449-1456.
22.	Lai M, Huijbers MG, Lancaster E, et al. Investigation of LGI1 as the antigen in limbic encephalitis previously attributed to potassium channels: a case series. Lancet Neurol, 2010, 9(8): 776-785.
23.	Petit-Pedrol M, Armangue T, Peng X, et al. Encephalitis with refractory seizures, status epilepticus, and antibodies to the GABAA receptor: a case series, characterisation of the antigen, and analysis of the effects of antibodies. Lancet Neurol, 2014, 13(3): 276-286.
24.	Spatola M, Petit-Pedrol M, Simabukuro MM, et al. Investigations in GABA(A) receptor antibody-associated encephalitis. Neurology, 2017, 88(11): 1012-1020.
25.	O'Connor K, Waters P, Komorowski L, et al. GABA(A) receptor autoimmunity: a multicenter experience. Neurology(R) neuroimmunology & neuroinflammation, 2019, 6(3): e552.
26.	Lancaster E, Lai M, Peng X, et al. Antibodies to the GABA(B) receptor in limbic encephalitis with seizures: case series and characterisation of the antigen. Lancet Neurol, 2010, 9(1): 67-76.
27.	H?ftberger R, Titulaer MJ, Sabater L, et al. Encephalitis and GABAB receptor antibodies: novel findings in a new case series of 20 patients. Neurology, 2013, 81(17): 1500-1506.
28.	Lin J, Li C, Li A, et al. Encephalitis with antibodies against the GABA(B) receptor: high mortality and risk factors. Frontiers in Neurology, 2019, 10: 1030.
29.	Yao L, Yue W, Xunyi W, et al. Clinical features and long-term outcomes of seizures associated with autoimmune encephalitis: A follow-up study in East China. Journal of Clinical Neuroscience, 2019, 68: 73-79.
30.	de Bruijn M, van Sonderen A, van Coevorden-Hameete MH, et al. Evaluation of seizure treatment in anti-LGI1, anti-NMDAR, and anti-GABA(B)R encephalitis. Neurology, 2019, 92(19): e2185-e2196.
31.	Trinka E, Cock H, Hesdorffer D, et al. A definition and classification of status epilepticus-Report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia, 2015, 56(10): 1515-1523.
32.	Obeso JA, Rothwell JC, Marsden CD. The spectrum of cortical myoclonus. From focal reflex jerks to spontaneous motor epilepsy. Brain, 1985, 108 ( Pt 1): 193-124.
33.	Dalmau J, Gleichman AJ, Hughes EG, et al. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol, 2008, 7(12): 1091-1098.
34.	Irani SR, Bera K, Waters P, et al. N-methyl-D-aspartate antibody encephalitis: temporal progression of clinical and paraclinical observations in a predominantly non-paraneoplastic disorder of both sexes. Brain, 2010, 133(Pt 6): 1655-1667.
35.	Chi X, Wang W, Huang C, et al. Risk factors for mortality in patients with anti-NMDA receptor encephalitis. Acta neurologica Scandinavica, 2017, 136(4): 298-304.
36.	Gultekin SH, Rosenfeld MR, Voltz R, et al. Paraneoplastic limbic encephalitis: neurological symptoms, immunological findings and tumour association in 50 patients. Brain, 2000, 123 ( Pt 7): 1481-1494.
37.	Lawn ND, Westmoreland BF, Kiely MJ, et al. Clinical, magnetic resonance imaging, and electroencephalographic findings in paraneoplastic limbic encephalitis. Mayo Clinic Proceedings, 2003, 78(11): 1363-1368.
38.	Spatola M, Novy J, Du Pasquier R, et al. Status epilepticus of inflammatory etiology: a cohort study. Neurology, 2015, 85(5): 464-470.
39.	Broadley J, Seneviratne U, Beech P, et al. Prognosticating autoimmune encephalitis: a systematic review. Journal of Autoimmunity, 2019, 96: 24-34.
40.	Lancaster E, Martinez-Hernandez E, Dalmau J. Encephalitis and antibodies to synaptic and neuronal cell surface proteins. Neurology, 2011, 77(2): 179-189.
41.	Liu X, Yan B, Wang R, et al. Seizure outcomes in patients with anti-NMDAR encephalitis: a follow-up study. Epilepsia, 2017, 58(12): 2104-2111.
42.	Celicanin M, Blaabjerg M, Maersk-Moller C, et al. Autoimmune encephalitis associated with voltage-gated potassium channels-complex and leucine-rich glioma-inactivated 1 antibodies - a national cohort study. European Journal of Neurology, 2017, 24(8): 999-1005.
43.	Flanagan EP, Kotsenas AL, Britton JW, et al. Basal ganglia T1 hyperintensity in LGI1-autoantibody faciobrachial dystonic seizures. Neurology(R) Neuroimmunology & Neuroinflammation, 2015, 2(6): e161.
44.	Feyissa AM, López Chiriboga AS, Britton JW. Antiepileptic drug therapy in patients with autoimmune epilepsy. Neurology(R) Neuroimmunology & Neuroinflammation, 2017, 4(4): e353.
45.	Irani SR, Michell AW, Lang B, et al. Faciobrachial dystonic seizures precede Lgi1 antibody limbic encephalitis. Annals of Neurology, 2011, 69(5): 892-900.
46.	Thompson J, Bi M, Murchison AG, et al. The importance of early immunotherapy in patients with faciobrachial dystonic seizures. Brain, 2018, 141(2): 348-356.
47.	Irani SR, Stagg CJ, Schott JM, et al. Faciobrachial dystonic seizures: the influence of immunotherapy on seizure control and prevention of cognitive impairment in a broadening phenotype. Brain, 2013, 136(Pt 10): 3151-3162.
48.	van Sonderen A, Roelen DL, Stoop JA, et al. Anti-LGI1 encephalitis is strongly associated with HLA-DR7 and HLA-DRB4. Annals of Neurology, 2017, 81(2): 193-198.
49.	Kim TJ, Lee ST, Moon J, et al. Anti-LGI1 encephalitis is associated with unique HLA subtypes. Annals of Neurology, 2017, 81(2): 183-192.
50.	Mueller SH, F?rber A, Prüss H, et al. Genetic predisposition in anti-LGI1 and anti-NMDA receptor encephalitis. Annals of Neurology, 2018, 83(4): 863-869.
51.	Shi YW, Min FL, Zhou D, et al. HLA-A*24: 02 as a common risk factor for antiepileptic drug-induced cutaneous adverse reactions. Neurology, 2017, 88(23): 2183-2191.
52.	Man CB, Kwan P, Baum L, et al. Association between HLA-B*1502 allele and antiepileptic drug-induced cutaneous reactions in Han Chinese. Epilepsia, 2007, 48(5): 1015-1018.
53.	McCormack M, Alfirevic A, Bourgeois S, et al. HLA-A*3101 and carbamazepine-induced hypersensitivity reactions in Europeans. The New England Journal of Medicine, 2011, 364(12): 1134-1143.
54.	Honnorat J, Didelot A, Karantoni E, et al. Autoimmune limbic encephalopathy and anti-Hu antibodies in children without cancer. Neurology, 2013, 80(24): 2226-2232.
55.	Malter MP, Helmstaedter C, Urbach H, et al. Antibodies to glutamic acid decarboxylase define a form of limbic encephalitis. Annals of Neurology, 2010, 67(4): 470-478.
56.	Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: position paper of the ILAE Commission for Classification and Terminology. Epilepsia, 2017, 58(4): 512-521.
57.	Dubey D, Alqallaf A, Hays R, et al. Neurological autoantibody prevalence in epilepsy of unknown etiology. JAMA Neurology, 2017, 74(4): 397-402.
58.	Schmitt SE, Pargeon K, Frechette ES, et al. Extreme delta brush: a unique EEG pattern in adults with anti-NMDA receptor encephalitis. Neurology, 2012, 79(11): 1094-1100.
59.	Jeannin-Mayer S, André-Obadia N, Rosenberg S, et al. EEG analysis in anti-NMDA receptor encephalitis: Description of typical patterns. Clinical Neurophysiology, 2019, 130(2): 289-296.
60.	Gillinder L, Warren N, Hartel G, et al. EEG findings in NMDA encephalitis - a systematic review. Seizure, 2019, 65: 20-24.
61.	Titulaer MJ, McCracken L, Gabilondo I, et al. Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study. Lancet Neurol, 2013, 12(2): 157-165.
62.	Dalmau J, Tüzün E, Wu HY, et al. Paraneoplastic anti-N-methyl-D-aspartate receptor encephalitis associated with ovarian teratoma. Annals of Neurology, 2007, 61(1): 25-36.
63.	Tüzün E, Zhou L, Baehring JM, et al. Evidence for antibody-mediated pathogenesis in anti-NMDAR encephalitis associated with ovarian teratoma. Acta Neuropathologica, 2009, 118(6): 737-743.
64.	Makuch M, Wilson R, Al-Diwani A, et al. N-methyl-D-aspartate receptor antibody production from germinal center reactions: Therapeutic implications. Annals of Neurology, 2018, 83(3): 553-561.
65.	Armangue T, Spatola M, Vlagea A, et al. Frequency, symptoms, risk factors, and outcomes of autoimmune encephalitis after herpes simplex encephalitis: a prospective observational study and retrospective analysis. Lancet Neurol, 2018, 17(9): 760-772.
66.	Williams TJ, Benavides DR, Patrice KA, et al. Association of autoimmune encephalitis with combined immune checkpoint inhibitor treatment for metastatic cancer. JAMA Neurology, 2016, 73(8): 928-933.
67.	Lee SK, Lee ST. The laboratory diagnosis of autoimmune encephalitis. Journal of Epilepsy Research, 2016, 6(2): 45-50.
68.	Martinez-Hernandez E, Horvath J, Shiloh-Malawsky Y, et al. Analysis of complement and plasma cells in the brain of patients with anti-NMDAR encephalitis. Neurology, 2011, 77(6): 589-593.
69.	Hughes EG, Peng X, Gleichman AJ, et al. Cellular and synaptic mechanisms of anti-NMDA receptor encephalitis. The Journal of Neuroscience, 2010, 30(17): 5866-5875.
70.	Gresa-Arribas N, Titulaer MJ, Torrents A, et al. Antibody titres at diagnosis and during follow-up of anti-NMDA receptor encephalitis: a retrospective study. Lancet Neurol, 2014, 13(2): 167-177.
71.	Vidarsson G, Dekkers G, Rispens T. IgG subclasses and allotypes: from structure to effector functions. Frontiers in Immunology, 2014, 5: 520.
72.	Dalmau J, Lancaster E, Martinez-Hernandez E, et al. Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis. Lancet Neurol, 2011, 10(1): 63-74.
73.	Dheen ST, Kaur C, Ling EA. Microglial activation and its implications in the brain diseases. Current Medicinal Chemistry, 2007, 14(11): 1189-1197.
74.	Town T, Nikolic V, Tan J. The microglial "activation" continuum: from innate to adaptive responses. Journal of Neuroinflammation, 2005, 2: 24.
75.	During MJ, Spencer DD. Extracellular hippocampal glutamate and spontaneous seizure in the conscious human brain. Lancet, 1993, 341(8861): 1607-1610.
76.	Eyo UB, Peng J, Swiatkowski P, et al. Neuronal hyperactivity recruits microglial processes via neuronal NMDA receptors and microglial P2Y12 receptors after status epilepticus. The Journal of Neuroscience, 2014, 34(32): 10528-10540.
77.	Manto M, Dalmau J, Didelot A, et al. In vivo effects of antibodies from patients with anti-NMDA receptor encephalitis: further evidence of synaptic glutamatergic dysfunction. Orphanet Journal of Rare Diseases, 2010, 5: 31.
78.	Moscato EH, Peng X, Jain A, et al. Acute mechanisms underlying antibody effects in anti-N-methyl-D-aspartate receptor encephalitis. Annals of Neurology, 2014, 76(1): 108-119.
79.	Platzer K, Lemke JR. GRIN1-Related Neurodevelopmental Disorder. In: Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJH, Stephens K, et al. GeneReviews(R). Seattle (WA), 1993.
80.	Hanada T. Ionotropic glutamate receptors in epilepsy: a review focusing on AMPA and NMDA Receptors. Biomolecules, 2020, 10(3).
81.	Finke C, Kopp UA, Scheel M, et al. Functional and structural brain changes in anti-N-methyl-D-aspartate receptor encephalitis. Annals of Neurology, 2013, 74(2): 284-296.
82.	Finke C, Kopp UA, Pajkert A, et al. Structural hippocampal damage following anti-N-Methyl-D-Aspartate receptor encephalitis. Biological Psychiatry, 2016, 79(9): 727-734.
83.	Finke C, Kopp UA, Prüss H, et al. Cognitive deficits following anti-NMDA receptor encephalitis. Journal of Neurology, Neurosurgery, and Psychiatry, 2012, 83(2): 195-198.
84.	Aurangzeb S, Symmonds M, Knight RK, et al. LGI1-antibody encephalitis is characterised by frequent, multifocal clinical and subclinical seizures. Seizure, 2017, 50: 14-17.
85.	Navarro V, Kas A, Apartis E, et al. Motor cortex and hippocampus are the two main cortical targets in LGI1-antibody encephalitis. Brain, 2016, 139(Pt 4): 1079-1093.
86.	Boesebeck F, Schwarz O, Dohmen B, et al. Faciobrachial dystonic seizures arise from cortico-subcortical abnormal brain areas. Journal of Neurology, 2013, 260(6): 1684-1686.
87.	Finke C, Prüss H, Heine J, et al. Evaluation of cognitive deficits and structural hippocampal damage in encephalitis with leucine-rich, glioma-inactivated 1 antibodies. JAMA Neurology, 2017, 74(1): 50-59.
88.	Irani SR, Alexander S, Waters P, et al. Antibodies to Kv1 potassium channel-complex proteins leucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 in limbic encephalitis, Morvan's syndrome and acquired neuromyotonia. Brain, 2010, 133(9): 2734-2748.
89.	Bien CG, Bien CI, Dogan Onugoren M, et al. Routine diagnostics for neural antibodies, clinical correlates, treatment and functional outcome. Journal of Neurology, 2020, 267(7): 2101-2114.
90.	Dalmau J, Geis C, Graus F. Autoantibodies to synaptic receptors and neuronal cell surface proteins in autoimmune diseases of the central nervous system. Physiological Reviews, 2017, 97(2): 839-887.
91.	Yamagata A, Fukai S. Insights into the mechanisms of epilepsy from structural biology of LGI1-ADAM22. Cellular and Molecular Life Sciences: CMLS, 2020, 77(2): 267-274.
92.	Petit-Pedrol M, Sell J, Planagumà J, et al. LGI1 antibodies alter Kv1.1 and AMPA receptors changing synaptic excitability, plasticity and memory. Brain, 2018, 141(11): 3144-3159.
93.	Ohkawa T, Fukata Y, Yamasaki M, et al. Autoantibodies to epilepsy-related LGI1 in limbic encephalitis neutralize LGI1-ADAM22 interaction and reduce synaptic AMPA receptors. The Journal of Neuroscience, 2013, 33(46): 18161-18174.
94.	Boronat A, Sabater L, Saiz A, et al. GABA(B) receptor antibodies in limbic encephalitis and anti-GAD-associated neurologic disorders. Neurology, 2011, 76(9): 795-800.
95.	Maureille A, Fenouil T, Joubert B, et al. Isolated seizures are a common early feature of paraneoplastic anti-GABA(B) receptor encephalitis. Journal of Neurology, 2019, 266(1): 195-206.
96.	Dogan Onugoren M, Deuretzbacher D, Haensch CA, et al. Limbic encephalitis due to GABAB and AMPA receptor antibodies: a case series. Journal of Neurology, Neurosurgery, and Psychiatry, 2015, 86(9): 965-972.
97.	Zhao XH, Yang X, Liu XW, et al. Clinical features and outcomes of Chinese patients with anti-γ-aminobutyric acid B receptor encephalitis. Experimental and Therapeutic Medicine, 2020, 20(1): 617-622.
98.	Benarroch EE. GABAB receptors: structure, functions, and clinical implications. Neurology, 2012, 78(8): 578-584.
99.	Nibber A, Mann EO, Pettingill P, et al. Pathogenic potential of antibodies to the GABA(B) receptor. Epilepsia Open, 2017, 2(3): 355-359.
100.	Frisullo G, Della Marca G, Mirabella M, et al. A human anti-neuronal autoantibody against GABA B receptor induces experimental autoimmune agrypnia. Experimental Neurology, 2007, 204(2): 808-818.
101.	Dalmau J, Graus F, Villarejo A, et al. Clinical analysis of anti-Ma2-associated encephalitis. Brain, 2004, 127(Pt 8): 1831-1844.
102.	Honnorat J, Cartalat-Carel S, Ricard D, et al. Onco-neural antibodies and tumour type determine survival and neurological symptoms in paraneoplastic neurological syndromes with Hu or CV2/CRMP5 antibodies. Journal of Neurology, Neurosurgery, and Psychiatry, 2009, 80(4): 412-416.
103.	Sillevis Smitt P, Grefkens J, de Leeuw B, et al. Survival and outcome in 73 anti-Hu positive patients with paraneoplastic encephalomyelitis/sensory neuronopathy. Journal of Neurology, 2002, 249(6): 745-753.
104.	Alamowitch S, Graus F, Uchuya M, et al. Limbic encephalitis and small cell lung cancer. Clinical and immunological features. Brain, 1997, 120 ( Pt 6): 923-928.
105.	Heine J, Ly LT, Lieker I, et al. Immunoadsorption or plasma exchange in the treatment of autoimmune encephalitis: a pilot study. Journal of neurology, 2016, 263(12): 2395-2402.
106.	Carre?o M, Bien CG, Asadi-Pooya AA, et al. Epilepsy surgery in drug resistant temporal lobe epilepsy associated with neuronal antibodies. Epilepsy Research, 2017, 129: 101-105.
107.	Baysal-Kirac L, Tuzun E, Erdag E, et al. Neuronal autoantibodies in epilepsy patients with peri-ictal autonomic findings. Journal of Neurology, 2016, 263(3): 455-466.
108.	Vanli-Yavuz EN, Erdag E, Tuzun E, et al. Neuronal autoantibodies in mesial temporal lobe epilepsy with hippocampal sclerosis. Journal of Neurology, Neurosurgery, and Psychiatry, 2016, 87(7): 684-692.
109.	Graus F, Saiz A, Dalmau J. GAD antibodies in neurological disorders - insights and challenges. Nat Rev Neurol, 2020, 16(7): 353-365.
110.	Lin YT, Yang X, Lv JW, et al. CXCL13 is a biomarker of anti-leucine-rich glioma-inactivated protein 1 encephalitis patients. Neuropsychiatric Disease and Treatment, 2019, 15: 2909-2915.
111.	Leypoldt F, H?ftberger R, Titulaer MJ, et al. Investigations on CXCL13 in anti-N-methyl-D-aspartate receptor encephalitis: a potential biomarker of treatment response. JAMA Neurology, 2015, 72(2): 180-186.
112.	Liba Z, Kayserova J, Elisak M, et al. Anti-N-methyl-D-aspartate receptor encephalitis: the clinical course in light of the chemokine and cytokine levels in cerebrospinal fluid. Journal of Neuroinflammation, 2016, 13(1): 55.
113.	Ulusoy C, Tüzün E, Kürtüncü M, et al. Comparison of the cytokine profiles of patients with neuronal-antibody-associated central nervous system disorders. The International Journal of Neuroscience, 2012, 122(6): 284-289.
114.	Campa M, Mansouri B, Warren R, et al. A review of biologic therapies targeting IL-23 and IL-17 for use in moderate-to-severe plaque psoriasis. Dermatology and Therapy, 2016, 6(1): 1-12.
115.	Lamb YN, Duggan ST. Ustekinumab: a review in moderate to severe crohn's disease. Drugs, 2017, 77(10): 1105-1114.
116.	Ari?o H, Armangué T, Petit-Pedrol M, et al. Anti-LGI1-associated cognitive impairment: Presentation and long-term outcome. Neurology, 2016, 87(8): 759-765.
117.	Ai P, Zhang X, Xie Z, et al. The HMGB1 is increased in CSF of patients with an Anti-NMDAR encephalitis. Acta Neurologica Scandinavica, 2018, 137(2): 277-282.
118.	Ichiyama T, Shoji H, Takahashi Y, et al. Cerebrospinal fluid levels of cytokines in non-herpetic acute limbic encephalitis: comparison with herpes simplex encephalitis. Cytokine, 2008, 44(1): 149-153.
119.	Leng SX, McElhaney JE, Walston JD, et al. ELISA and multiplex technologies for cytokine measurement in inflammation and aging research. The Journals of Gerontology Series A, Biological Sciences and Medical Sciences, 2008, 63(8): 879-884.
120.	Wu D, Milutinovic MD, Walt DR. Single molecule array (Simoa) assay with optimal antibody pairs for cytokine detection in human serum samples. The Analyst, 2015, 140(18): 6277-6282.
121.	Hirsch LJ, Gaspard N, van Baalen A, et al. Proposed consensus definitions for new-onset refractory status epilepticus (NORSE), febrile infection-related epilepsy syndrome (FIRES), and related conditions. Epilepsia, 2018, 59(4): 739-744.
122.	Nabbout R. FIRES and IHHE: delineation of the syndromes . Epilepsia, 2013, 54(Suppl 6): 54-56.
123.	Mikaeloff Y, Jambaqué I, Hertz-Pannier L, et al. Devastating epileptic encephalopathy in school-aged children (DESC): a pseudo encephalitis. Epilepsy research, 2006, 69(1): 67-79.
124.	Sakuma H, Fukumizu M, Kohyama J. [Efficacy of anticonvulsants on acute encephalitis with refractory, repetitive partial seizures (AERRPS). Brain and Development, 2001, 33(5): 385-390.
125.	Bien CG, Granata T, Antozzi C, et al. Pathogenesis, diagnosis and treatment of Rasmussen encephalitis: a European consensus statement. Brain, 2005, 128(Pt 3): 454-471.
126.	Gaspard N, Hirsch LJ, Sculier C, et al. New-onset refractory status epilepticus (NORSE) and febrile infection-related epilepsy syndrome (FIRES): state of the art and perspectives. Epilepsia, 2018, 59(4): 745-752.
127.	Alparslan C, Kamit-Can F, An?l AB, et al. Febrile infection-related epilepsy syndrome (FIRES) treated with immunomodulation in an 8-year-old boy and review of the literature. The Turkish Journal of Pediatrics, 2017, 59(4): 463-466.
128.	Jun JS, Lee ST, Kim R, et al. Tocilizumab treatment for new onset refractory status epilepticus. Annals of Neurology, 2018, 84(6): 940-945.
129.	van Baalen A, H?usler M, Plecko-Startinig B, et al. Febrile infection-related epilepsy syndrome without detectable autoantibodies and response to immunotherapy: a case series and discussion of epileptogenesis in FIRES. Neuropediatrics, 2012, 43(4): 209-216.
130.	Li Y, Uccelli A, Laxer KD, et al. Local-clonal expansion of infiltrating T lymphocytes in chronic encephalitis of Rasmussen. Journal of Immunology, 1997, 158(3): 1428-1437.
131.	Pardo CA, Vining EP, Guo L, et al. The pathology of Rasmussen syndrome: stages of cortical involvement and neuropathological studies in 45 hemispherectomies. Epilepsia, 2004, 45(5): 516-526.
132.	Wang D, Blümcke I, Gui Q, et al. Clinico-pathological investigations of Rasmussen encephalitis suggest multifocal disease progression and associated focal cortical dysplasia. Epileptic Disorders, 2013, 15(1): 32-43.
133.	Howell KB, Katanyuwong K, Mackay MT, et al. Long-term follow-up of febrile infection-related epilepsy syndrome. Epilepsia, 2012, 53(1): 101-110.
134.	Sakuma H, Awaya Y, Shiomi M, et al. Acute encephalitis with refractory, repetitive partial seizures (AERRPS): a peculiar form of childhood encephalitis. Acta Neurologica Scandinavica, 2010, 121(4): 251-256.
135.	Bien CG, Widman G, Urbach H, et al. The natural history of Rasmussen's encephalitis. Brain, 2002, 125(Pt 8): 1751-1759.
136.	Cabrera Kang CM, Gaspard N, LaRoche SM, et al. Survey of the diagnostic and therapeutic approach to new-onset refractory status epilepticus. Seizure, 2017, 46: 24-30.
137.	Sculier C, Gaspard N. New onset refractory status epilepticus (NORSE). Seizure, 2019, 68: 72-78.
138.	Li J, Saldivar C, Maganti RK. Plasma exchange in cryptogenic new onset refractory status epilepticus. Seizure, 2013, 22(1): 70-73.
139.	Khawaja AM, DeWolfe JL, Miller DW, et al. New-onset refractory status epilepticus (NORSE)-The potential role for immunotherapy. Epilepsy & Behavior, 2015, 47: 17-23.
140.	Iizuka T, Kanazawa N, Kaneko J, et al. Cryptogenic NORSE: Its distinctive clinical features and response to immunotherapy. Neurology(R) neuroimmunology & neuroinflammation, 2017, 4(6): e396.
141.	Gall CR, Jumma O, Mohanraj R. Five cases of new onset refractory status epilepticus (NORSE) syndrome: outcomes with early immunotherapy. Seizure, 2013, 22(3): 217-220.
142.	Caraballo RH, Reyes G, Avaria MF, et al. Febrile infection-related epilepsy syndrome: a study of 12 patients. Seizure, 2013, 22(7): 553-559.
143.	Sato Y, Numata-Uematsu Y, Uematsu M, et al. Acute encephalitis with refractory, repetitive partial seizures: Pathological findings and a new therapeutic approach using tacrolimus. Brain & Development, 2016, 38(8): 772-776.
144.	van Baalen A, H?usler M, Boor R, et al. Febrile infection-related epilepsy syndrome (FIRES): a nonencephalitic encephalopathy in childhood. Epilepsia, 2010, 51(7): 1323-1328.
145.	Dilena R, Mauri E, Aronica E, et al. Therapeutic effect of Anakinra in the relapsing chronic phase of febrile infection-related epilepsy syndrome. Epilepsia Open, 2019, 4(2): 344-350.
146.	Costello DJ, Kilbride RD, Cole AJ. Cryptogenic New Onset Refractory Status Epilepticus (NORSE) in adults-Infectious or not? Journal of the Neurological Sciences, 2009, 277(1-2): 26-31.
147.	Wilder-Smith EP, Lim EC, Teoh HL, et al. The NORSE (new-onset refractory status epilepticus) syndrome: defining a disease entity. Annals of the Academy of Medicine, 2005, 34(7): 417-420.
148.	Wakamoto H, Takahashi Y, Ebihara T, et al. An immunologic case study of acute encephalitis with refractory, repetitive partial seizures. Brain & Development, 2012, 34(9): 763-767.
149.	Kothur K, Bandodkar S, Wienholt L, et al. Etiology is the key determinant of neuroinflammation in epilepsy: Elevation of cerebrospinal fluid cytokines and chemokines in febrile infection-related epilepsy syndrome and febrile status epilepticus. Epilepsia, 2019, 60(8): 1678-1688.
150.	Clarkson BD S, LaFrance-Corey RG, Kahoud RJ, et al. Functional deficiency in endogenous interleukin-1 receptor antagonist in patients with febrile infection-related epilepsy syndrome. Annals of Neurology, 2019, 85(4): 526-537.
151.	Kenney-Jung DL, Vezzani A, Kahoud RJ, et al. Febrile infection-related epilepsy syndrome treated with anakinra. Annals of Neurology, 2016, 80(6): 939-945.
152.	Sakuma H, Tanuma N, Kuki I, et al. Intrathecal overproduction of proinflammatory cytokines and chemokines in febrile infection-related refractory status epilepticus. Journal of Nneurology, Neurosurgery, and Psychiatry, 2015, 86(7): 820-822.
153.	Vezzani A, Maroso M, Balosso S, et al. IL-1 receptor/Toll-like receptor signaling in infection, inflammation, stress and neurodegeneration couples hyperexcitability and seizures. Brain, Behavior, and Immunity, 2011, 25(7): 1281-1289.
154.	Gallentine WB, Shinnar S, Hesdorffer DC, et al. Plasma cytokines associated with febrile status epilepticus in children: A potential biomarker for acute hippocampal injury. Epilepsia, 2017, 58(6): 1102-1111.
155.	Manicone AM, McGuire JK. Matrix metalloproteinases as modulators of inflammation. Seminars in Cell & Developmental Biology, 2008, 19(1): 34-41.
156.	Lewis DV, Shinnar S, Hesdorffer DC, et al. Hippocampal sclerosis after febrile status epilepticus: the FEBSTAT study. Annals of Neurology, 2014, 75(2): 178-185.
157.	Tr?scher A R, Wimmer I, Quemada-Garrido L, et al. Microglial nodules provide the environment for pathogenic T cells in human encephalitis. Acta Neuropathologica, 2019, 137(4): 619-635.
158.	Schwab N, Bien CG, Waschbisch A, et al. CD8+ T-cell clones dominate brain infiltrates in Rasmussen encephalitis and persist in the periphery. Brain, 2009, 132(Pt 5): 1236-1246.
159.	Ramaswamy V, Walsh JG, Sinclair DB, et al. Inflammasome induction in Rasmussen's encephalitis: cortical and associated white matter pathogenesis. Journal of Neuroinflammation, 2013, 10: 152.
160.	Bien CG, Bauer J, Deckwerth TL, et al. Destruction of neurons by cytotoxic T cells: a new pathogenic mechanism in Rasmussen's encephalitis. Annals of Neurology, 2002, 51(3): 311-318.
161.	Owens GC, Huynh MN, Chang JW, et al. Differential expression of interferon-γ and chemokine genes distinguishes Rasmussen encephalitis from cortical dysplasia and provides evidence for an early Th1 immune response. Journal of Neuroinflammation, 2013, 10: 56.
162.	Guo H, Callaway JB, Ting J P. Inflammasomes: mechanism of action, role in disease, and therapeutics. Nature Medicine, 2015, 21(7): 677-687.
163.	Takahashi Y, Mine J, Kubota Y, et al. A substantial number of Rasmussen syndrome patients have increased IgG, CD4+ T cells, TNFalpha, and Granzyme B in CSF. Epilepsia, 2009, 50(6): 1419-1431.
164.	Sawada M, Kondo N, Suzumura A, et al. Production of tumor necrosis factor-alpha by microglia and astrocytes in culture. Brain Research, 1989, 491(2): 394-397.
165.	Samanci B, Tektürk P, Tüzün E, et al. Neuronal autoantibodies in patients with Rasmussen's encephalitis. Epileptic Disorders, 2016, 18(2): 204-210.
166.	Nibber A, Clover L, Pettingill P, et al. Antibodies to AMPA receptors in Rasmussen's encephalitis. European Journal of Paediatric Neurology, 2016, 20(2): 222-227.
167.	Cepeda C, Chang JW, Owens GC, et al. In Rasmussen encephalitis, hemichannels associated with microglial activation are linked to cortical pyramidal neuron coupling: a possible mechanism for cellular hyperexcitability. CNS Neuroscience & Therapeutics, 2015, 21(2): 152-163.
168.	Takahashi Y, Yamazaki E, Mine J, et al. Immunomodulatory therapy versus surgery for Rasmussen syndrome in early childhood. Brain & Development, 2013, 35(8): 778-785.
169.	Bittner S, Simon OJ, G?bel K, et al. Rasmussen encephalitis treated with natalizumab. Neurology, 2013, 81(4): 395-397.
170.	Lagarde S, Villeneuve N, Trébuchon A, et al. Anti-tumor necrosis factor alpha therapy (adalimumab) in Rasmussen's encephalitis: An open pilot study. Epilepsia, 2016, 57(6): 956-966.
171.	Thilo B, Stingele R, Knudsen K, et al. A case of Rasmussen encephalitis treated with rituximab. Nat Rev Neurol, 2009, 5(8): 458-462.
172.	El Tawil S, Morris R, Mullatti N, et al. Adult onset Rasmussen's encephalitis associated with reflex language induced seizures responsive to Rituximab therapy. Seizure, 2016, 42: 60-62.
173.	Bien CG, Schramm J. Treatment of Rasmussen encephalitis half a century after its initial description: promising prospects and a dilemma. Epilepsy Research, 2009, 86(2-3): 101-112.
174.	Khan NL, Jeffree MA, Good C, et al. Histopathology of VGKC antibody–associated limbic encephalitis. Neurology, 2009, 72(19): 1703-1705.
175.	Park DC, Murman DL, Perry KD, et al. An autopsy case of limbic encephalitis with voltage‐gated potassium channel antibodies. European Journal of Neurology, 2007, 14(10): e5-e6.
176.	Dunstan EJ, Winer JB. Autoimmune limbic encephalitis causing fits, rapidly progressive confusion and hyponatraemia. Age and Ageing, 2006, 35(5): 536-537.
177.	Juhász C, Buth A, Chugani DC, et al. Successful surgical treatment of an inflammatory lesion associated with new-onset refractory status epilepticus. Neurosurgical Focus, 2013, 34(6): E5.
178.	Al Nimer F, Jelcic I, Kempf C, et al. Phenotypic and functional complexity of brain-infiltrating T cells in Rasmussen encephalitis. Neurology-Neuroimmunology Neuroinflammation, 2018, 5(1).
179.	Choi J, Nordli DR, Alden TD, et al. Cellular injury and neuroinflammation in children with chronic intractable epilepsy. Journal of Neuroinflammation, 2009, 6(1): 1-14.

1. Wandinger KP, Leypoldt F, Junker R. Autoantibody-Mediated Encephalitis. Dtsch Arztebl Int, 2018, 115(40): 666-673.
2. Spatola M, Dalmau J. Seizures and risk of epilepsy in autoimmune and other inflammatory encephalitis. Curr Opin Neurol, 2017, 30(3): 345-353.
3. Nabbout R, Vezzani A, Dulac O, et al. Acute encephalopathy with inflammation-mediated status epilepticus. Lancet Neurol, 2011, 10(1): 99-108.
4. Gaspard N, Foreman BP, Alvarez V, et al. New-onset refractory status epilepticus: Etiology, clinical features, and outcome. Neurology, 2015, 85(18): 1604-1613.
5. Kramer U, Chi CS, Lin KL, et al. Febrile infection-related epilepsy syndrome (FIRES): pathogenesis, treatment, and outcome: a multicenter study on 77 children. Epilepsia, 2011, 52(11): 1956-1965.
6. Vezzani A, Balosso S, Ravizza T. Neuroinflammatory pathways as treatment targets and biomarkers in epilepsy. Nat Rev Neurol, 2019, 15(8): 459-472.
7. Vezzani A, Dingledine R, Rossetti AO. Immunity and inflammation in status epilepticus and its sequelae: possibilities for therapeutic application. Expert review of neurotherapeutics, 2015, 15(9): 1081-1092.
8. van Vliet EA, Aronica E, Vezzani A, et al. Neuroinflammatory pathways as treatment targets and biomarker candidates in epilepsy: emerging evidence from preclinical and clinical studies. Neuropathology and applied neurobiology, 2018, 44(1): 91-111.
9. Holtkamp M, Othman J, Buchheim K, et al. Predictors and prognosis of refractory status epilepticus treated in a neurological intensive care unit. Journal of neurology, neurosurgery, and psychiatry, 2005, 76(4): 534-539.
10. Santamarina E, Gonzalez M, Toledo M, et al. Prognosis of status epilepticus (SE): relationship between SE duration and subsequent development of epilepsy. Epilepsy & Behavior, 2015, 49: 138-140.
11. Hesdorffer DC, Logroscino G, Cascino G, et al. Risk of unprovoked seizure after acute symptomatic seizure: effect of status epilepticus. Annals of neurology, 1998, 44(6): 908-912.
12. Ruiz-García R, Martínez-Hernández E, Saiz A, et al. The diagnostic value of onconeural antibodies depends on how they are tested. Frontiers in immunology, 2020, 11: 1482.
13. Geis C, Planagumà J, Carre?o M, et al. Autoimmune seizures and epilepsy. The Journal of clinical investigation, 2019, 129(3): 926-940.
14. Graus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol, 2016, 15(4): 391-404.
15. Tüzün E, Dalmau J. Limbic encephalitis and variants: classification, diagnosis and treatment. The neurologist, 2007, 13(5): 261-271.
16. Esposito S, Principi N, Calabresi P, et al. An evolving redefinition of autoimmune encephalitis. Autoimmunity reviews, 2019, 18(2): 155-163.
17. Quek AML, O'Toole O. Autoimmune epilepsy: the evolving science of neural autoimmunity and its impact on epilepsy management. Seminars in neurology, 2018, 38(3): 290-302.
18. Bien CG, Vincent A, Barnett MH, et al. Immunopathology of autoantibody-associated encephalitides: clues for pathogenesis. Brain: a journal of neurology, 2012, 135(Pt 5): 1622-1638.
19. Rada A, Birnbacher R, Gobbi C, et al. Seizures associated with antibodies against cell surface antigens are acute symptomatic and not indicative of epilepsy: insights from long-term data. Journal of neurology, 2021, 268(3): 1059-1069.
20. Steriade C, Britton J, Dale RC, et al. Acute symptomatic seizures secondary to autoimmune encephalitis and autoimmune-associated epilepsy: Conceptual definitions. Epilepsia, 2020, 61(7): 1341-1351.
21. van Sonderen A, Thijs RD, Coenders EC, et al. Anti-LGI1 encephalitis: clinical syndrome and long-term follow-up. Neurology, 2016, 87(14): 1449-1456.
22. Lai M, Huijbers MG, Lancaster E, et al. Investigation of LGI1 as the antigen in limbic encephalitis previously attributed to potassium channels: a case series. Lancet Neurol, 2010, 9(8): 776-785.
23. Petit-Pedrol M, Armangue T, Peng X, et al. Encephalitis with refractory seizures, status epilepticus, and antibodies to the GABAA receptor: a case series, characterisation of the antigen, and analysis of the effects of antibodies. Lancet Neurol, 2014, 13(3): 276-286.
24. Spatola M, Petit-Pedrol M, Simabukuro MM, et al. Investigations in GABA(A) receptor antibody-associated encephalitis. Neurology, 2017, 88(11): 1012-1020.
25. O'Connor K, Waters P, Komorowski L, et al. GABA(A) receptor autoimmunity: a multicenter experience. Neurology(R) neuroimmunology & neuroinflammation, 2019, 6(3): e552.
26. Lancaster E, Lai M, Peng X, et al. Antibodies to the GABA(B) receptor in limbic encephalitis with seizures: case series and characterisation of the antigen. Lancet Neurol, 2010, 9(1): 67-76.
27. H?ftberger R, Titulaer MJ, Sabater L, et al. Encephalitis and GABAB receptor antibodies: novel findings in a new case series of 20 patients. Neurology, 2013, 81(17): 1500-1506.
28. Lin J, Li C, Li A, et al. Encephalitis with antibodies against the GABA(B) receptor: high mortality and risk factors. Frontiers in Neurology, 2019, 10: 1030.
29. Yao L, Yue W, Xunyi W, et al. Clinical features and long-term outcomes of seizures associated with autoimmune encephalitis: A follow-up study in East China. Journal of Clinical Neuroscience, 2019, 68: 73-79.
30. de Bruijn M, van Sonderen A, van Coevorden-Hameete MH, et al. Evaluation of seizure treatment in anti-LGI1, anti-NMDAR, and anti-GABA(B)R encephalitis. Neurology, 2019, 92(19): e2185-e2196.
31. Trinka E, Cock H, Hesdorffer D, et al. A definition and classification of status epilepticus-Report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia, 2015, 56(10): 1515-1523.
32. Obeso JA, Rothwell JC, Marsden CD. The spectrum of cortical myoclonus. From focal reflex jerks to spontaneous motor epilepsy. Brain, 1985, 108 ( Pt 1): 193-124.
33. Dalmau J, Gleichman AJ, Hughes EG, et al. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol, 2008, 7(12): 1091-1098.
34. Irani SR, Bera K, Waters P, et al. N-methyl-D-aspartate antibody encephalitis: temporal progression of clinical and paraclinical observations in a predominantly non-paraneoplastic disorder of both sexes. Brain, 2010, 133(Pt 6): 1655-1667.
35. Chi X, Wang W, Huang C, et al. Risk factors for mortality in patients with anti-NMDA receptor encephalitis. Acta neurologica Scandinavica, 2017, 136(4): 298-304.
36. Gultekin SH, Rosenfeld MR, Voltz R, et al. Paraneoplastic limbic encephalitis: neurological symptoms, immunological findings and tumour association in 50 patients. Brain, 2000, 123 ( Pt 7): 1481-1494.
37. Lawn ND, Westmoreland BF, Kiely MJ, et al. Clinical, magnetic resonance imaging, and electroencephalographic findings in paraneoplastic limbic encephalitis. Mayo Clinic Proceedings, 2003, 78(11): 1363-1368.
38. Spatola M, Novy J, Du Pasquier R, et al. Status epilepticus of inflammatory etiology: a cohort study. Neurology, 2015, 85(5): 464-470.
39. Broadley J, Seneviratne U, Beech P, et al. Prognosticating autoimmune encephalitis: a systematic review. Journal of Autoimmunity, 2019, 96: 24-34.
40. Lancaster E, Martinez-Hernandez E, Dalmau J. Encephalitis and antibodies to synaptic and neuronal cell surface proteins. Neurology, 2011, 77(2): 179-189.
41. Liu X, Yan B, Wang R, et al. Seizure outcomes in patients with anti-NMDAR encephalitis: a follow-up study. Epilepsia, 2017, 58(12): 2104-2111.
42. Celicanin M, Blaabjerg M, Maersk-Moller C, et al. Autoimmune encephalitis associated with voltage-gated potassium channels-complex and leucine-rich glioma-inactivated 1 antibodies - a national cohort study. European Journal of Neurology, 2017, 24(8): 999-1005.
43. Flanagan EP, Kotsenas AL, Britton JW, et al. Basal ganglia T1 hyperintensity in LGI1-autoantibody faciobrachial dystonic seizures. Neurology(R) Neuroimmunology & Neuroinflammation, 2015, 2(6): e161.
44. Feyissa AM, López Chiriboga AS, Britton JW. Antiepileptic drug therapy in patients with autoimmune epilepsy. Neurology(R) Neuroimmunology & Neuroinflammation, 2017, 4(4): e353.
45. Irani SR, Michell AW, Lang B, et al. Faciobrachial dystonic seizures precede Lgi1 antibody limbic encephalitis. Annals of Neurology, 2011, 69(5): 892-900.
46. Thompson J, Bi M, Murchison AG, et al. The importance of early immunotherapy in patients with faciobrachial dystonic seizures. Brain, 2018, 141(2): 348-356.
47. Irani SR, Stagg CJ, Schott JM, et al. Faciobrachial dystonic seizures: the influence of immunotherapy on seizure control and prevention of cognitive impairment in a broadening phenotype. Brain, 2013, 136(Pt 10): 3151-3162.
48. van Sonderen A, Roelen DL, Stoop JA, et al. Anti-LGI1 encephalitis is strongly associated with HLA-DR7 and HLA-DRB4. Annals of Neurology, 2017, 81(2): 193-198.
49. Kim TJ, Lee ST, Moon J, et al. Anti-LGI1 encephalitis is associated with unique HLA subtypes. Annals of Neurology, 2017, 81(2): 183-192.
50. Mueller SH, F?rber A, Prüss H, et al. Genetic predisposition in anti-LGI1 and anti-NMDA receptor encephalitis. Annals of Neurology, 2018, 83(4): 863-869.
51. Shi YW, Min FL, Zhou D, et al. HLA-A*24: 02 as a common risk factor for antiepileptic drug-induced cutaneous adverse reactions. Neurology, 2017, 88(23): 2183-2191.
52. Man CB, Kwan P, Baum L, et al. Association between HLA-B*1502 allele and antiepileptic drug-induced cutaneous reactions in Han Chinese. Epilepsia, 2007, 48(5): 1015-1018.
53. McCormack M, Alfirevic A, Bourgeois S, et al. HLA-A*3101 and carbamazepine-induced hypersensitivity reactions in Europeans. The New England Journal of Medicine, 2011, 364(12): 1134-1143.
54. Honnorat J, Didelot A, Karantoni E, et al. Autoimmune limbic encephalopathy and anti-Hu antibodies in children without cancer. Neurology, 2013, 80(24): 2226-2232.
55. Malter MP, Helmstaedter C, Urbach H, et al. Antibodies to glutamic acid decarboxylase define a form of limbic encephalitis. Annals of Neurology, 2010, 67(4): 470-478.
56. Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: position paper of the ILAE Commission for Classification and Terminology. Epilepsia, 2017, 58(4): 512-521.
57. Dubey D, Alqallaf A, Hays R, et al. Neurological autoantibody prevalence in epilepsy of unknown etiology. JAMA Neurology, 2017, 74(4): 397-402.
58. Schmitt SE, Pargeon K, Frechette ES, et al. Extreme delta brush: a unique EEG pattern in adults with anti-NMDA receptor encephalitis. Neurology, 2012, 79(11): 1094-1100.
59. Jeannin-Mayer S, André-Obadia N, Rosenberg S, et al. EEG analysis in anti-NMDA receptor encephalitis: Description of typical patterns. Clinical Neurophysiology, 2019, 130(2): 289-296.
60. Gillinder L, Warren N, Hartel G, et al. EEG findings in NMDA encephalitis - a systematic review. Seizure, 2019, 65: 20-24.
61. Titulaer MJ, McCracken L, Gabilondo I, et al. Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study. Lancet Neurol, 2013, 12(2): 157-165.
62. Dalmau J, Tüzün E, Wu HY, et al. Paraneoplastic anti-N-methyl-D-aspartate receptor encephalitis associated with ovarian teratoma. Annals of Neurology, 2007, 61(1): 25-36.
63. Tüzün E, Zhou L, Baehring JM, et al. Evidence for antibody-mediated pathogenesis in anti-NMDAR encephalitis associated with ovarian teratoma. Acta Neuropathologica, 2009, 118(6): 737-743.
64. Makuch M, Wilson R, Al-Diwani A, et al. N-methyl-D-aspartate receptor antibody production from germinal center reactions: Therapeutic implications. Annals of Neurology, 2018, 83(3): 553-561.
65. Armangue T, Spatola M, Vlagea A, et al. Frequency, symptoms, risk factors, and outcomes of autoimmune encephalitis after herpes simplex encephalitis: a prospective observational study and retrospective analysis. Lancet Neurol, 2018, 17(9): 760-772.
66. Williams TJ, Benavides DR, Patrice KA, et al. Association of autoimmune encephalitis with combined immune checkpoint inhibitor treatment for metastatic cancer. JAMA Neurology, 2016, 73(8): 928-933.
67. Lee SK, Lee ST. The laboratory diagnosis of autoimmune encephalitis. Journal of Epilepsy Research, 2016, 6(2): 45-50.
68. Martinez-Hernandez E, Horvath J, Shiloh-Malawsky Y, et al. Analysis of complement and plasma cells in the brain of patients with anti-NMDAR encephalitis. Neurology, 2011, 77(6): 589-593.
69. Hughes EG, Peng X, Gleichman AJ, et al. Cellular and synaptic mechanisms of anti-NMDA receptor encephalitis. The Journal of Neuroscience, 2010, 30(17): 5866-5875.
70. Gresa-Arribas N, Titulaer MJ, Torrents A, et al. Antibody titres at diagnosis and during follow-up of anti-NMDA receptor encephalitis: a retrospective study. Lancet Neurol, 2014, 13(2): 167-177.
71. Vidarsson G, Dekkers G, Rispens T. IgG subclasses and allotypes: from structure to effector functions. Frontiers in Immunology, 2014, 5: 520.
72. Dalmau J, Lancaster E, Martinez-Hernandez E, et al. Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis. Lancet Neurol, 2011, 10(1): 63-74.
73. Dheen ST, Kaur C, Ling EA. Microglial activation and its implications in the brain diseases. Current Medicinal Chemistry, 2007, 14(11): 1189-1197.
74. Town T, Nikolic V, Tan J. The microglial "activation" continuum: from innate to adaptive responses. Journal of Neuroinflammation, 2005, 2: 24.
75. During MJ, Spencer DD. Extracellular hippocampal glutamate and spontaneous seizure in the conscious human brain. Lancet, 1993, 341(8861): 1607-1610.
76. Eyo UB, Peng J, Swiatkowski P, et al. Neuronal hyperactivity recruits microglial processes via neuronal NMDA receptors and microglial P2Y12 receptors after status epilepticus. The Journal of Neuroscience, 2014, 34(32): 10528-10540.
77. Manto M, Dalmau J, Didelot A, et al. In vivo effects of antibodies from patients with anti-NMDA receptor encephalitis: further evidence of synaptic glutamatergic dysfunction. Orphanet Journal of Rare Diseases, 2010, 5: 31.
78. Moscato EH, Peng X, Jain A, et al. Acute mechanisms underlying antibody effects in anti-N-methyl-D-aspartate receptor encephalitis. Annals of Neurology, 2014, 76(1): 108-119.
79. Platzer K, Lemke JR. GRIN1-Related Neurodevelopmental Disorder. In: Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJH, Stephens K, et al. GeneReviews(R). Seattle (WA), 1993.
80. Hanada T. Ionotropic glutamate receptors in epilepsy: a review focusing on AMPA and NMDA Receptors. Biomolecules, 2020, 10(3).
81. Finke C, Kopp UA, Scheel M, et al. Functional and structural brain changes in anti-N-methyl-D-aspartate receptor encephalitis. Annals of Neurology, 2013, 74(2): 284-296.
82. Finke C, Kopp UA, Pajkert A, et al. Structural hippocampal damage following anti-N-Methyl-D-Aspartate receptor encephalitis. Biological Psychiatry, 2016, 79(9): 727-734.
83. Finke C, Kopp UA, Prüss H, et al. Cognitive deficits following anti-NMDA receptor encephalitis. Journal of Neurology, Neurosurgery, and Psychiatry, 2012, 83(2): 195-198.
84. Aurangzeb S, Symmonds M, Knight RK, et al. LGI1-antibody encephalitis is characterised by frequent, multifocal clinical and subclinical seizures. Seizure, 2017, 50: 14-17.
85. Navarro V, Kas A, Apartis E, et al. Motor cortex and hippocampus are the two main cortical targets in LGI1-antibody encephalitis. Brain, 2016, 139(Pt 4): 1079-1093.
86. Boesebeck F, Schwarz O, Dohmen B, et al. Faciobrachial dystonic seizures arise from cortico-subcortical abnormal brain areas. Journal of Neurology, 2013, 260(6): 1684-1686.
87. Finke C, Prüss H, Heine J, et al. Evaluation of cognitive deficits and structural hippocampal damage in encephalitis with leucine-rich, glioma-inactivated 1 antibodies. JAMA Neurology, 2017, 74(1): 50-59.
88. Irani SR, Alexander S, Waters P, et al. Antibodies to Kv1 potassium channel-complex proteins leucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 in limbic encephalitis, Morvan's syndrome and acquired neuromyotonia. Brain, 2010, 133(9): 2734-2748.
89. Bien CG, Bien CI, Dogan Onugoren M, et al. Routine diagnostics for neural antibodies, clinical correlates, treatment and functional outcome. Journal of Neurology, 2020, 267(7): 2101-2114.
90. Dalmau J, Geis C, Graus F. Autoantibodies to synaptic receptors and neuronal cell surface proteins in autoimmune diseases of the central nervous system. Physiological Reviews, 2017, 97(2): 839-887.
91. Yamagata A, Fukai S. Insights into the mechanisms of epilepsy from structural biology of LGI1-ADAM22. Cellular and Molecular Life Sciences: CMLS, 2020, 77(2): 267-274.
92. Petit-Pedrol M, Sell J, Planagumà J, et al. LGI1 antibodies alter Kv1.1 and AMPA receptors changing synaptic excitability, plasticity and memory. Brain, 2018, 141(11): 3144-3159.
93. Ohkawa T, Fukata Y, Yamasaki M, et al. Autoantibodies to epilepsy-related LGI1 in limbic encephalitis neutralize LGI1-ADAM22 interaction and reduce synaptic AMPA receptors. The Journal of Neuroscience, 2013, 33(46): 18161-18174.
94. Boronat A, Sabater L, Saiz A, et al. GABA(B) receptor antibodies in limbic encephalitis and anti-GAD-associated neurologic disorders. Neurology, 2011, 76(9): 795-800.
95. Maureille A, Fenouil T, Joubert B, et al. Isolated seizures are a common early feature of paraneoplastic anti-GABA(B) receptor encephalitis. Journal of Neurology, 2019, 266(1): 195-206.
96. Dogan Onugoren M, Deuretzbacher D, Haensch CA, et al. Limbic encephalitis due to GABAB and AMPA receptor antibodies: a case series. Journal of Neurology, Neurosurgery, and Psychiatry, 2015, 86(9): 965-972.
97. Zhao XH, Yang X, Liu XW, et al. Clinical features and outcomes of Chinese patients with anti-γ-aminobutyric acid B receptor encephalitis. Experimental and Therapeutic Medicine, 2020, 20(1): 617-622.
98. Benarroch EE. GABAB receptors: structure, functions, and clinical implications. Neurology, 2012, 78(8): 578-584.
99. Nibber A, Mann EO, Pettingill P, et al. Pathogenic potential of antibodies to the GABA(B) receptor. Epilepsia Open, 2017, 2(3): 355-359.
100. Frisullo G, Della Marca G, Mirabella M, et al. A human anti-neuronal autoantibody against GABA B receptor induces experimental autoimmune agrypnia. Experimental Neurology, 2007, 204(2): 808-818.
101. Dalmau J, Graus F, Villarejo A, et al. Clinical analysis of anti-Ma2-associated encephalitis. Brain, 2004, 127(Pt 8): 1831-1844.
102. Honnorat J, Cartalat-Carel S, Ricard D, et al. Onco-neural antibodies and tumour type determine survival and neurological symptoms in paraneoplastic neurological syndromes with Hu or CV2/CRMP5 antibodies. Journal of Neurology, Neurosurgery, and Psychiatry, 2009, 80(4): 412-416.
103. Sillevis Smitt P, Grefkens J, de Leeuw B, et al. Survival and outcome in 73 anti-Hu positive patients with paraneoplastic encephalomyelitis/sensory neuronopathy. Journal of Neurology, 2002, 249(6): 745-753.
104. Alamowitch S, Graus F, Uchuya M, et al. Limbic encephalitis and small cell lung cancer. Clinical and immunological features. Brain, 1997, 120 ( Pt 6): 923-928.
105. Heine J, Ly LT, Lieker I, et al. Immunoadsorption or plasma exchange in the treatment of autoimmune encephalitis: a pilot study. Journal of neurology, 2016, 263(12): 2395-2402.
106. Carre?o M, Bien CG, Asadi-Pooya AA, et al. Epilepsy surgery in drug resistant temporal lobe epilepsy associated with neuronal antibodies. Epilepsy Research, 2017, 129: 101-105.
107. Baysal-Kirac L, Tuzun E, Erdag E, et al. Neuronal autoantibodies in epilepsy patients with peri-ictal autonomic findings. Journal of Neurology, 2016, 263(3): 455-466.
108. Vanli-Yavuz EN, Erdag E, Tuzun E, et al. Neuronal autoantibodies in mesial temporal lobe epilepsy with hippocampal sclerosis. Journal of Neurology, Neurosurgery, and Psychiatry, 2016, 87(7): 684-692.
109. Graus F, Saiz A, Dalmau J. GAD antibodies in neurological disorders - insights and challenges. Nat Rev Neurol, 2020, 16(7): 353-365.
110. Lin YT, Yang X, Lv JW, et al. CXCL13 is a biomarker of anti-leucine-rich glioma-inactivated protein 1 encephalitis patients. Neuropsychiatric Disease and Treatment, 2019, 15: 2909-2915.
111. Leypoldt F, H?ftberger R, Titulaer MJ, et al. Investigations on CXCL13 in anti-N-methyl-D-aspartate receptor encephalitis: a potential biomarker of treatment response. JAMA Neurology, 2015, 72(2): 180-186.
112. Liba Z, Kayserova J, Elisak M, et al. Anti-N-methyl-D-aspartate receptor encephalitis: the clinical course in light of the chemokine and cytokine levels in cerebrospinal fluid. Journal of Neuroinflammation, 2016, 13(1): 55.
113. Ulusoy C, Tüzün E, Kürtüncü M, et al. Comparison of the cytokine profiles of patients with neuronal-antibody-associated central nervous system disorders. The International Journal of Neuroscience, 2012, 122(6): 284-289.
114. Campa M, Mansouri B, Warren R, et al. A review of biologic therapies targeting IL-23 and IL-17 for use in moderate-to-severe plaque psoriasis. Dermatology and Therapy, 2016, 6(1): 1-12.
115. Lamb YN, Duggan ST. Ustekinumab: a review in moderate to severe crohn's disease. Drugs, 2017, 77(10): 1105-1114.
116. Ari?o H, Armangué T, Petit-Pedrol M, et al. Anti-LGI1-associated cognitive impairment: Presentation and long-term outcome. Neurology, 2016, 87(8): 759-765.
117. Ai P, Zhang X, Xie Z, et al. The HMGB1 is increased in CSF of patients with an Anti-NMDAR encephalitis. Acta Neurologica Scandinavica, 2018, 137(2): 277-282.
118. Ichiyama T, Shoji H, Takahashi Y, et al. Cerebrospinal fluid levels of cytokines in non-herpetic acute limbic encephalitis: comparison with herpes simplex encephalitis. Cytokine, 2008, 44(1): 149-153.
119. Leng SX, McElhaney JE, Walston JD, et al. ELISA and multiplex technologies for cytokine measurement in inflammation and aging research. The Journals of Gerontology Series A, Biological Sciences and Medical Sciences, 2008, 63(8): 879-884.
120. Wu D, Milutinovic MD, Walt DR. Single molecule array (Simoa) assay with optimal antibody pairs for cytokine detection in human serum samples. The Analyst, 2015, 140(18): 6277-6282.
121. Hirsch LJ, Gaspard N, van Baalen A, et al. Proposed consensus definitions for new-onset refractory status epilepticus (NORSE), febrile infection-related epilepsy syndrome (FIRES), and related conditions. Epilepsia, 2018, 59(4): 739-744.
122. Nabbout R. FIRES and IHHE: delineation of the syndromes . Epilepsia, 2013, 54(Suppl 6): 54-56.
123. Mikaeloff Y, Jambaqué I, Hertz-Pannier L, et al. Devastating epileptic encephalopathy in school-aged children (DESC): a pseudo encephalitis. Epilepsy research, 2006, 69(1): 67-79.
124. Sakuma H, Fukumizu M, Kohyama J. [Efficacy of anticonvulsants on acute encephalitis with refractory, repetitive partial seizures (AERRPS). Brain and Development, 2001, 33(5): 385-390.
125. Bien CG, Granata T, Antozzi C, et al. Pathogenesis, diagnosis and treatment of Rasmussen encephalitis: a European consensus statement. Brain, 2005, 128(Pt 3): 454-471.
126. Gaspard N, Hirsch LJ, Sculier C, et al. New-onset refractory status epilepticus (NORSE) and febrile infection-related epilepsy syndrome (FIRES): state of the art and perspectives. Epilepsia, 2018, 59(4): 745-752.
127. Alparslan C, Kamit-Can F, An?l AB, et al. Febrile infection-related epilepsy syndrome (FIRES) treated with immunomodulation in an 8-year-old boy and review of the literature. The Turkish Journal of Pediatrics, 2017, 59(4): 463-466.
128. Jun JS, Lee ST, Kim R, et al. Tocilizumab treatment for new onset refractory status epilepticus. Annals of Neurology, 2018, 84(6): 940-945.
129. van Baalen A, H?usler M, Plecko-Startinig B, et al. Febrile infection-related epilepsy syndrome without detectable autoantibodies and response to immunotherapy: a case series and discussion of epileptogenesis in FIRES. Neuropediatrics, 2012, 43(4): 209-216.
130. Li Y, Uccelli A, Laxer KD, et al. Local-clonal expansion of infiltrating T lymphocytes in chronic encephalitis of Rasmussen. Journal of Immunology, 1997, 158(3): 1428-1437.
131. Pardo CA, Vining EP, Guo L, et al. The pathology of Rasmussen syndrome: stages of cortical involvement and neuropathological studies in 45 hemispherectomies. Epilepsia, 2004, 45(5): 516-526.
132. Wang D, Blümcke I, Gui Q, et al. Clinico-pathological investigations of Rasmussen encephalitis suggest multifocal disease progression and associated focal cortical dysplasia. Epileptic Disorders, 2013, 15(1): 32-43.
133. Howell KB, Katanyuwong K, Mackay MT, et al. Long-term follow-up of febrile infection-related epilepsy syndrome. Epilepsia, 2012, 53(1): 101-110.
134. Sakuma H, Awaya Y, Shiomi M, et al. Acute encephalitis with refractory, repetitive partial seizures (AERRPS): a peculiar form of childhood encephalitis. Acta Neurologica Scandinavica, 2010, 121(4): 251-256.
135. Bien CG, Widman G, Urbach H, et al. The natural history of Rasmussen's encephalitis. Brain, 2002, 125(Pt 8): 1751-1759.
136. Cabrera Kang CM, Gaspard N, LaRoche SM, et al. Survey of the diagnostic and therapeutic approach to new-onset refractory status epilepticus. Seizure, 2017, 46: 24-30.
137. Sculier C, Gaspard N. New onset refractory status epilepticus (NORSE). Seizure, 2019, 68: 72-78.
138. Li J, Saldivar C, Maganti RK. Plasma exchange in cryptogenic new onset refractory status epilepticus. Seizure, 2013, 22(1): 70-73.
139. Khawaja AM, DeWolfe JL, Miller DW, et al. New-onset refractory status epilepticus (NORSE)-The potential role for immunotherapy. Epilepsy & Behavior, 2015, 47: 17-23.
140. Iizuka T, Kanazawa N, Kaneko J, et al. Cryptogenic NORSE: Its distinctive clinical features and response to immunotherapy. Neurology(R) neuroimmunology & neuroinflammation, 2017, 4(6): e396.
141. Gall CR, Jumma O, Mohanraj R. Five cases of new onset refractory status epilepticus (NORSE) syndrome: outcomes with early immunotherapy. Seizure, 2013, 22(3): 217-220.
142. Caraballo RH, Reyes G, Avaria MF, et al. Febrile infection-related epilepsy syndrome: a study of 12 patients. Seizure, 2013, 22(7): 553-559.
143. Sato Y, Numata-Uematsu Y, Uematsu M, et al. Acute encephalitis with refractory, repetitive partial seizures: Pathological findings and a new therapeutic approach using tacrolimus. Brain & Development, 2016, 38(8): 772-776.
144. van Baalen A, H?usler M, Boor R, et al. Febrile infection-related epilepsy syndrome (FIRES): a nonencephalitic encephalopathy in childhood. Epilepsia, 2010, 51(7): 1323-1328.
145. Dilena R, Mauri E, Aronica E, et al. Therapeutic effect of Anakinra in the relapsing chronic phase of febrile infection-related epilepsy syndrome. Epilepsia Open, 2019, 4(2): 344-350.
146. Costello DJ, Kilbride RD, Cole AJ. Cryptogenic New Onset Refractory Status Epilepticus (NORSE) in adults-Infectious or not? Journal of the Neurological Sciences, 2009, 277(1-2): 26-31.
147. Wilder-Smith EP, Lim EC, Teoh HL, et al. The NORSE (new-onset refractory status epilepticus) syndrome: defining a disease entity. Annals of the Academy of Medicine, 2005, 34(7): 417-420.
148. Wakamoto H, Takahashi Y, Ebihara T, et al. An immunologic case study of acute encephalitis with refractory, repetitive partial seizures. Brain & Development, 2012, 34(9): 763-767.
149. Kothur K, Bandodkar S, Wienholt L, et al. Etiology is the key determinant of neuroinflammation in epilepsy: Elevation of cerebrospinal fluid cytokines and chemokines in febrile infection-related epilepsy syndrome and febrile status epilepticus. Epilepsia, 2019, 60(8): 1678-1688.
150. Clarkson BD S, LaFrance-Corey RG, Kahoud RJ, et al. Functional deficiency in endogenous interleukin-1 receptor antagonist in patients with febrile infection-related epilepsy syndrome. Annals of Neurology, 2019, 85(4): 526-537.
151. Kenney-Jung DL, Vezzani A, Kahoud RJ, et al. Febrile infection-related epilepsy syndrome treated with anakinra. Annals of Neurology, 2016, 80(6): 939-945.
152. Sakuma H, Tanuma N, Kuki I, et al. Intrathecal overproduction of proinflammatory cytokines and chemokines in febrile infection-related refractory status epilepticus. Journal of Nneurology, Neurosurgery, and Psychiatry, 2015, 86(7): 820-822.
153. Vezzani A, Maroso M, Balosso S, et al. IL-1 receptor/Toll-like receptor signaling in infection, inflammation, stress and neurodegeneration couples hyperexcitability and seizures. Brain, Behavior, and Immunity, 2011, 25(7): 1281-1289.
154. Gallentine WB, Shinnar S, Hesdorffer DC, et al. Plasma cytokines associated with febrile status epilepticus in children: A potential biomarker for acute hippocampal injury. Epilepsia, 2017, 58(6): 1102-1111.
155. Manicone AM, McGuire JK. Matrix metalloproteinases as modulators of inflammation. Seminars in Cell & Developmental Biology, 2008, 19(1): 34-41.
156. Lewis DV, Shinnar S, Hesdorffer DC, et al. Hippocampal sclerosis after febrile status epilepticus: the FEBSTAT study. Annals of Neurology, 2014, 75(2): 178-185.
157. Tr?scher A R, Wimmer I, Quemada-Garrido L, et al. Microglial nodules provide the environment for pathogenic T cells in human encephalitis. Acta Neuropathologica, 2019, 137(4): 619-635.
158. Schwab N, Bien CG, Waschbisch A, et al. CD8+ T-cell clones dominate brain infiltrates in Rasmussen encephalitis and persist in the periphery. Brain, 2009, 132(Pt 5): 1236-1246.
159. Ramaswamy V, Walsh JG, Sinclair DB, et al. Inflammasome induction in Rasmussen's encephalitis: cortical and associated white matter pathogenesis. Journal of Neuroinflammation, 2013, 10: 152.
160. Bien CG, Bauer J, Deckwerth TL, et al. Destruction of neurons by cytotoxic T cells: a new pathogenic mechanism in Rasmussen's encephalitis. Annals of Neurology, 2002, 51(3): 311-318.
161. Owens GC, Huynh MN, Chang JW, et al. Differential expression of interferon-γ and chemokine genes distinguishes Rasmussen encephalitis from cortical dysplasia and provides evidence for an early Th1 immune response. Journal of Neuroinflammation, 2013, 10: 56.
162. Guo H, Callaway JB, Ting J P. Inflammasomes: mechanism of action, role in disease, and therapeutics. Nature Medicine, 2015, 21(7): 677-687.
163. Takahashi Y, Mine J, Kubota Y, et al. A substantial number of Rasmussen syndrome patients have increased IgG, CD4+ T cells, TNFalpha, and Granzyme B in CSF. Epilepsia, 2009, 50(6): 1419-1431.
164. Sawada M, Kondo N, Suzumura A, et al. Production of tumor necrosis factor-alpha by microglia and astrocytes in culture. Brain Research, 1989, 491(2): 394-397.
165. Samanci B, Tektürk P, Tüzün E, et al. Neuronal autoantibodies in patients with Rasmussen's encephalitis. Epileptic Disorders, 2016, 18(2): 204-210.
166. Nibber A, Clover L, Pettingill P, et al. Antibodies to AMPA receptors in Rasmussen's encephalitis. European Journal of Paediatric Neurology, 2016, 20(2): 222-227.
167. Cepeda C, Chang JW, Owens GC, et al. In Rasmussen encephalitis, hemichannels associated with microglial activation are linked to cortical pyramidal neuron coupling: a possible mechanism for cellular hyperexcitability. CNS Neuroscience & Therapeutics, 2015, 21(2): 152-163.
168. Takahashi Y, Yamazaki E, Mine J, et al. Immunomodulatory therapy versus surgery for Rasmussen syndrome in early childhood. Brain & Development, 2013, 35(8): 778-785.
169. Bittner S, Simon OJ, G?bel K, et al. Rasmussen encephalitis treated with natalizumab. Neurology, 2013, 81(4): 395-397.
170. Lagarde S, Villeneuve N, Trébuchon A, et al. Anti-tumor necrosis factor alpha therapy (adalimumab) in Rasmussen's encephalitis: An open pilot study. Epilepsia, 2016, 57(6): 956-966.
171. Thilo B, Stingele R, Knudsen K, et al. A case of Rasmussen encephalitis treated with rituximab. Nat Rev Neurol, 2009, 5(8): 458-462.
172. El Tawil S, Morris R, Mullatti N, et al. Adult onset Rasmussen's encephalitis associated with reflex language induced seizures responsive to Rituximab therapy. Seizure, 2016, 42: 60-62.
173. Bien CG, Schramm J. Treatment of Rasmussen encephalitis half a century after its initial description: promising prospects and a dilemma. Epilepsy Research, 2009, 86(2-3): 101-112.
174. Khan NL, Jeffree MA, Good C, et al. Histopathology of VGKC antibody–associated limbic encephalitis. Neurology, 2009, 72(19): 1703-1705.
175. Park DC, Murman DL, Perry KD, et al. An autopsy case of limbic encephalitis with voltage‐gated potassium channel antibodies. European Journal of Neurology, 2007, 14(10): e5-e6.
176. Dunstan EJ, Winer JB. Autoimmune limbic encephalitis causing fits, rapidly progressive confusion and hyponatraemia. Age and Ageing, 2006, 35(5): 536-537.
177. Juhász C, Buth A, Chugani DC, et al. Successful surgical treatment of an inflammatory lesion associated with new-onset refractory status epilepticus. Neurosurgical Focus, 2013, 34(6): E5.
178. Al Nimer F, Jelcic I, Kempf C, et al. Phenotypic and functional complexity of brain-infiltrating T cells in Rasmussen encephalitis. Neurology-Neuroimmunology Neuroinflammation, 2018, 5(1).
179. Choi J, Nordli DR, Alden TD, et al. Cellular injury and neuroinflammation in children with chronic intractable epilepsy. Journal of Neuroinflammation, 2009, 6(1): 1-14.

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