Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review

Rapidly progressive dementia (RPD) is a heterogeneous group of diseases characterized by cognitive impairment and other neurological disorders developed in a short span of fewer than 2 years. Currently viewed as new and infrequent entities, most medical personnel have little understanding of it. Nev...

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Autores:: Hurtado González, Carlos Alberto
Ospina Otalvaro, Sebastian
Marmolejo Escobar, Carlos Steven
Quebrada Mera, Karen Julieth
Gutiérrez Lenis, Paola Andrea

Tipo de recurso:: Article of investigation

Fecha de publicación:: 2022

Institución:: Universidad Cooperativa de Colombia

Repositorio:: Repositorio UCC

Idioma:: eng

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repository_id_str
dc.title.none.fl_str_mv	Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review
title	Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review
spellingShingle	Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review Rapidly progressive dementia Voltage-gated potassium channel complex NMDAR Encephalitis Creutzfeldt-Jakob disease
title_short	Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review
title_full	Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review
title_fullStr	Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review
title_full_unstemmed	Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review
title_sort	Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review
dc.creator.fl_str_mv	Hurtado González, Carlos Alberto Ospina Otalvaro, Sebastian Marmolejo Escobar, Carlos Steven Quebrada Mera, Karen Julieth Gutiérrez Lenis, Paola Andrea
dc.contributor.author.none.fl_str_mv	Hurtado González, Carlos Alberto Ospina Otalvaro, Sebastian Marmolejo Escobar, Carlos Steven Quebrada Mera, Karen Julieth Gutiérrez Lenis, Paola Andrea
dc.contributor.researchgroup.none.fl_str_mv	SEMINEC
dc.subject.proposal.none.fl_str_mv	Rapidly progressive dementia Voltage-gated potassium channel complex NMDAR Encephalitis Creutzfeldt-Jakob disease
topic	Rapidly progressive dementia Voltage-gated potassium channel complex NMDAR Encephalitis Creutzfeldt-Jakob disease
description	Rapidly progressive dementia (RPD) is a heterogeneous group of diseases characterized by cognitive impairment and other neurological disorders developed in a short span of fewer than 2 years. Currently viewed as new and infrequent entities, most medical personnel have little understanding of it. Nevertheless, they significantly compromise many patients’ quality of life. Here, we drive 3 clinical cases that evolve as RPD with different etiologies. Case 1: 70-year-old woman presented to the emergency with neuropsychiatric syndrome for 18 days. The researchers identified inflammatory cerebrospinal fluid (CSF), protein 14-3-3-positive T-tau protein, MRI: T2 and FLAIR hyperintensities in bilateral caudate nuclei with diffusion restriction, EEG shows a generalized periodic pattern with triphasic wave morphology. Case 2: 29-yearold man with cognitive impairment and faciobrachial dystonia seizure. The diagnosis was confirmed by achieving elevated antibodies against voltage-gated potassium channels. Case 3: A 49-year-old woman with encephalopathy and myoclonic seizures; EEG and MRI showed subtle changes. The patient also had a normal CSF but a positive CBA serologic NMDA-R antibody test. We described fundamental aspects of RPD to allow made differential diagnoses in patients with cognitive impairment and encephalopathy. Establishing an early and accurate diagnosis can benefit patients with RPD etiologies that are treatable and even reversible, decreasing in morbidity and mortality.
publishDate	2022
dc.date.issued.none.fl_str_mv	2022-11
dc.date.accessioned.none.fl_str_mv	2024-02-20T17:00:10Z
dc.date.available.none.fl_str_mv	2024-02-20T17:00:10Z
dc.type.none.fl_str_mv	Artículos Científicos
dc.type.hasVersion.none.fl_str_mv	info:eu-repo/semantics/publishedVersion
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dc.type.content.none.fl_str_mv	Text
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dc.identifier.citation.none.fl_str_mv	Clavijo, C. A., Portilla Buenaventura, A. M., Benavides Albornoz, G. S., Muñoz Cabrera, J. J., Murillo Reyes, M. C., Chauvez Gallego, A., Hurtado González, C. A., Ospina Otalvaro, S., Marmolejo Escobar, C. S., Quebrada Mera, K. J., Lenis, P. A. G., Arango García, L. M., & Lucumí, A. (2022). Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review. Case Reports in Neurology, 14(3), 441–455. https://doi.org/10.1159/000525701
dc.identifier.uri.none.fl_str_mv	https://hdl.handle.net/20.500.12494/54993
dc.identifier.doi.none.fl_str_mv	10.1159/000525701
dc.identifier.eissn.none.fl_str_mv	1662680X
identifier_str_mv	Clavijo, C. A., Portilla Buenaventura, A. M., Benavides Albornoz, G. S., Muñoz Cabrera, J. J., Murillo Reyes, M. C., Chauvez Gallego, A., Hurtado González, C. A., Ospina Otalvaro, S., Marmolejo Escobar, C. S., Quebrada Mera, K. J., Lenis, P. A. G., Arango García, L. M., & Lucumí, A. (2022). Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review. Case Reports in Neurology, 14(3), 441–455. https://doi.org/10.1159/000525701 10.1159/000525701 1662680X
url	https://hdl.handle.net/20.500.12494/54993
dc.language.iso.none.fl_str_mv	eng
language	eng
dc.relation.citationendpage.none.fl_str_mv	463
dc.relation.citationstartpage.none.fl_str_mv	449
dc.relation.citationvolume.none.fl_str_mv	14
dc.relation.ispartofjournal.none.fl_str_mv	Case Reports in Neurology
dc.relation.references.none.fl_str_mv	Datri L, Quiroga J, Reisin R, Rojas G, Young P. Deterioro cognitivo rápidamente evolutivo. Análisis de 6 casos Rapidly progressive dementia; 2018 Mar. Geschwind MD, Shu H, Haman A, Sejvar JJ, Miller BL. Rapidly progressive dementia. Ann Neurol. 2008;64(1): 97–108 Lancaster E, Dalmau J. Neuronal autoantigens-pathogenesis, associated disorders, and antibody testing; 2012. Frost B, Diamond MI. Prion-like mechanisms in neurodegenerative diseases. Nat Rev Neurosci. 2010;11(3): 155–9. Ganor Y, Goldberg-Stern H, Amrom D, Lerman-Sagie T, Teichberg VI, Pelled D, et al. Autoimmune epilepsy: some epilepsy patients harbor autoantibodies to glutamate receptors and dsDNA on both sides of the bloodbrain barrier, which may kill neurons and decrease in brain fluids after hemispherotomy. Clin Dev Immunol. 2004 Sep–Dec;11(3–4):241–52. Brenner T, Sills GJ, Hart Y, Howell S, Waters P, Brodie MJ, et al. Prevalence of neurologic autoantibodies in cohorts of patients with new and established epilepsy. Epilepsia. 2013 Jun;54(6):1028–35 Prado CAC, Gallego AC. Autoimmune epilepsy—a new goal of science: report two cases in the San Jose Hospital, Bogota, Colombia. J Neurol Stroke. 2019;9(3):129–32. Kim MO, Geschwind MD. Clinical update of Jakob-Creutzfeldt disease. Curr Opin Neurol. 2015;28(3):302–10. Munné Díaz C, Grau Solà M, Torreño Sánchez M. Enfermedad de Creutzfeldt-jacob. Rev Científica la Soc Española Enfermería Neurológica [Internet]. Medicina en español. 2013 Jan 1 [cited 2020 Aug 27];37(1):29–32. Sanchez-Juan P, Green A, Ladogana A, Cuadrado-Corrales N, Sáanchez-Valle R, Mitrováa E, et al. CSF tests in the differential diagnosis of Creutzfeldt-Jakob disease. Neurology. 2006 Aug 22;67(4):637–43. Collins SJ, Sanchez-Juan P, Masters CL, Klug GM, van Duijn C, Poleggi A, et al. Determinants of diagnostic investigation sensitivities across the clinical spectrum of sporadic Creutzfeldt-Jakob disease. Brain. 2006 Sep; 129(Pt 9):2278–87. Epub 2006 Jul 1. Puoti G, Bizzi A, Forloni G, Safar JG, Tagliavini F, Gambetti P. Sporadic human prion diseases: molecular insights and diagnosis. Lancet Neurol. 2012;11(7):618–28. Zerr I, Pocchiari M, Collins S, Brandel JP, de Pedro Cuesta J, Knight RS, et al. Analysis of EEG and CSF 14-3-3 proteins as aids to the diagnosis of Creutzfeldt-Jakob disease. Neurology. 2000;55(6):811–5. van Sonderen A, Thijs RD, Coenders EC, Jiskoot LC, Sanchez E, de Bruijn MA, et al. Anti-LGI1 encephalitis: clinical syndrome and long-term follow-up. Neurology. 2016 Oct 4;87(14):1449–56. Epub 2016 Sep 2. Irani SR, Michell AW, Lang B, Pettingill P, Waters P, Johnson MR, et al. Faciobrachial dystonic seizures precede Lgi1 antibody limbic encephalitis. Ann Neurol. 2011 May;69(5):892–900. Epub 2011 Mar 17. Ekizoglu E, Tuzun E, Woodhall M, Lang B, Jacobson L, Icoz S, et al. Investigation of neuronal autoantibodies in two different focal epilepsy syndromes. Epilepsia. 2014;55(3):414–22 Liimatainen S, Peltola J, Hietaharju A, Sabater L, Lang B. Lack of antibodies to NMDAR or VGKC-complex in GAD and cardiolipin antibody-positive refractory epilepsy. Epilepsy Res. 2014 Mar;108(3):592–6. Epub 2014 Jan 6. Lai M, Huijbers MG, Lancaster E, Graus F, Bataller L, Balice-Gordon R, et al. Investigation of LGI1 as the antigen in limbic encephalitis previously attributed to potassium channels: a case series. Lancet Neurol. 2010;9:776–85. Lancaster E, Huijbers MG, Bar V, Boronat A, Wong A, Martinez-Hernandez E, et al. Investigations of Caspr2, an autoantigen of encephalitis and neuromyotonia. Ann Neurol. 2011;69:303–11. Klein CJ, Lennon VA, Aston PA, McKeonO’Toole O, O’Toole A, Quek A, et al. Insights from LGI1 and CASPR2 potassium channel complex autoantibody subtyping. JAMA Neurol. 2013;70:229–34. Irani R, Alexander R, Waters P, Kleopa KA, Pettingill P, Zuliani L, et al. Antibodies to Kv1 potassium channelcomplex proteins leucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 in limbic encephalitis, Morvan’s syndrome and acquired neuromyotonia. Brain. 2010;133:2734–48. Montojo MT, Petit-Pedrol M, Graus F, Dalmau J. Clinical spectrum and diagnostic value of antibodies against the potassium channel related protein complex. Neurologia. 2015;30(5):295–301 Fukata Y, Lovero KL, Iwanaga T, Watanabe A, Yokoi N, Tabuchi K, et al. Disruption of LGI1-linked synaptic complex causes abnormal synaptic transmission and epilepsy. Proc Natl Acad Sci U S A. 2010;107:3799–804. Yu YE, Wen L, Silva J, Li Z, Head K, Sossey-Alaoui K, et al. Lgi1 null mutant mice exhibit myoclonic seizures and CA1 neuronal hyperexcitability. Hum Mol Genet. 2010;19:1702–11. Titulaer MJ, McCracken L, Gabilondo I, Armangué T, Glaser C, Iizuka T, et al. Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study. Lancet Neurol. 2013;12:157–65. Iwasaki Y, Tatsumi S, Mimuro M, Kitamoto T, Hashizume Y, Yoshida M. Relation between clinical findings and progression of cerebral cortical pathology in MM1-type sporadic Creutzfeldt-Jakob disease: proposed staging of cerebral cortical pathology. J Neurol Sci. 2014 Jun 15;341(1–2):97–104. Iwasaki Y. Creutzfeldt-Jakob disease [Internet]. Neuropathology. 2017 Apr 1 [cited 2020 Nov 8];37(2):174–88. http://doi.wiley.com/10.1111/neup.12355. Otto M, Wiltfang J, Tumani H, Zerr I, Lantsch M, Kornhuber J, et al. Elevated levels of tau-protein in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease [Internet]. Neurosci Lett. 1997 Apr 11 [cited 2020 Nov 8];225(3):210–2. Muayqil T, Gronseth G, Camicioli R. Evidence-based guideline: diagnostic accuracy of CSF 14-3-3 protein in sporadic creutzfeldt-jakob disease: report of the guideline development subcommittee of the American academy of neurology [Internet]. Neurology. 2012 Oct 2 [cited 2020 Nov 8];79(14):1499–506 Geschwind MD, Potter CA, Sattavat M, Garcia PA, Rosen HJ, Miller BL, et al. Correlating DWI MRI with pathological and other features of Jakob-Creutzfeldt disease. Alzheimer Dis Assoc Disord. 2009 Jan–Mar;23(1):82–7. Will RG, Ironside JW. Sporadic and infectious human prion diseases. Cold Spring Harb Perspect Med. 2017 Jan 3 [cited 2020 Nov 8];7(1):a024364. Moreno-Madrigal LG, Ernesto-Díaz A, Oikawa-Sakaguchi VM. Encefalitis paraneoplásica. Acta Méd Grupo Ángeles [Revista en La Internet]. 2017;15(2):139–42. Gillinder L, Warren N, Hartel G, Dionisio S, O'Gorman C. EEG findings in NMDA encephalitis: a systematic review. Seizure. 2019;65:20–4. Reyes Botero G, Uribe Uribe CS, Hernández Ortiz OE, Ciro J, Guerra A, Dalmau Obrador J. Encefalitis paraneoplásica por anticuerpos contra el receptor de NMDA. Remisión completa después de la resección de un teratoma ovárico. RevNeurol. 2011;52(09):536–40. Guanyabens-Buscà N, Casado-Ruiz V, Giné-Serven E, Palomeras E, Muriana D, Boix-Quintana E, et al. Encefalitis antirreceptor de NMDA. Diagnóstico y tratamiento precoz en pacientes con sintomatología psicótica agudasubaguda. Rev Neurol. 2019;68(01):18–22.
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spelling	Hurtado González, Carlos AlbertoOspina Otalvaro, SebastianMarmolejo Escobar, Carlos StevenQuebrada Mera, Karen JuliethGutiérrez Lenis, Paola Andrea SEMINEC2024-02-20T17:00:10Z2024-02-20T17:00:10Z2022-11Clavijo, C. A., Portilla Buenaventura, A. M., Benavides Albornoz, G. S., Muñoz Cabrera, J. J., Murillo Reyes, M. C., Chauvez Gallego, A., Hurtado González, C. A., Ospina Otalvaro, S., Marmolejo Escobar, C. S., Quebrada Mera, K. J., Lenis, P. A. G., Arango García, L. M., & Lucumí, A. (2022). Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review. Case Reports in Neurology, 14(3), 441–455. https://doi.org/10.1159/000525701https://hdl.handle.net/20.500.12494/5499310.1159/0005257011662680XRapidly progressive dementia (RPD) is a heterogeneous group of diseases characterized by cognitive impairment and other neurological disorders developed in a short span of fewer than 2 years. Currently viewed as new and infrequent entities, most medical personnel have little understanding of it. Nevertheless, they significantly compromise many patients’ quality of life. Here, we drive 3 clinical cases that evolve as RPD with different etiologies. Case 1: 70-year-old woman presented to the emergency with neuropsychiatric syndrome for 18 days. The researchers identified inflammatory cerebrospinal fluid (CSF), protein 14-3-3-positive T-tau protein, MRI: T2 and FLAIR hyperintensities in bilateral caudate nuclei with diffusion restriction, EEG shows a generalized periodic pattern with triphasic wave morphology. Case 2: 29-yearold man with cognitive impairment and faciobrachial dystonia seizure. The diagnosis was confirmed by achieving elevated antibodies against voltage-gated potassium channels. Case 3: A 49-year-old woman with encephalopathy and myoclonic seizures; EEG and MRI showed subtle changes. The patient also had a normal CSF but a positive CBA serologic NMDA-R antibody test. We described fundamental aspects of RPD to allow made differential diagnoses in patients with cognitive impairment and encephalopathy. Establishing an early and accurate diagnosis can benefit patients with RPD etiologies that are treatable and even reversible, decreasing in morbidity and mortality.La demencia rápidamente progresiva (DPR) es un grupo heterogéneo de enfermedades caracterizadas por deterioro cognitivo y otros trastornos neurológicos que se desarrollan en un corto lapso de menos de 2 años. Consideradas actualmente como entidades nuevas y poco frecuentes, la mayoría del personal médico tiene poco conocimiento al respecto. Sin embargo, comprometen significativamente la calidad de vida de muchos pacientes. Aquí manejamos 3 casos clínicos que evolucionan como DPR con diferentes etiologías. Caso 1: Mujer de 70 años que acudió a urgencias con síndrome neuropsiquiátrico de 18 días de evolución. Los investigadores identificaron líquido cefalorraquídeo (LCR) inflamatorio, proteína T-tau positiva 14-3-3, MRI: hiperintensidades T2 y FLAIR en núcleos caudados bilaterales con restricción de difusión, el EEG muestra un patrón periódico generalizado con morfología de onda trifásica. Caso 2: Hombre de 29 años con deterioro cognitivo y convulsión por distonía faciobraquial. El diagnóstico se confirmó al alcanzar anticuerpos elevados contra los canales de potasio dependientes de voltaje. Caso 3: Mujer de 49 años con encefalopatía y crisis mioclónicas; EEG y MRI mostraron cambios sutiles. El paciente también tenía un LCR normal pero una prueba serológica de anticuerpos NMDA-R CBA positiva. Describimos aspectos fundamentales del DPR para permitir realizar diagnósticos diferenciales en pacientes con deterioro cognitivo y encefalopatía. Establecer un diagnóstico temprano y preciso puede beneficiar a los pacientes con etiologías de EPR que son tratables e incluso reversibles, disminuyendo la morbilidad y la mortalidad.Patologías neurodegenerativas y neuropsiquíatricas15 p.application/pdfengUniversidad Cooperativa de Colombia, Facultad de Ciencias Sociales, Psicología, CaliCalihttps://creativecommons.org/licenses/by-nd/4.0/info:eu-repo/semantics/closedAccessAtribución-SinDerivadas 4.0 Internacional (CC BY-ND 4.0)http://purl.org/coar/access_right/c_14cbhttps://bibliotecadigital.ucc.edu.co/permalink/57UCC_INST/17b7oqh/cdi_crossref_primary_10_1159_000525701Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative ReviewArtículos Científicosinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_2df8fbb1http://purl.org/coar/version/c_970fb48d4fbd8a85Textinfo:eu-repo/semantics/articlehttp://purl.org/redcol/resource_type/ARTinfo:eu-repo/semantics/publishedVersion46344914Case Reports in NeurologyDatri L, Quiroga J, Reisin R, Rojas G, Young P. Deterioro cognitivo rápidamente evolutivo. Análisis de 6 casos Rapidly progressive dementia; 2018 Mar.Geschwind MD, Shu H, Haman A, Sejvar JJ, Miller BL. Rapidly progressive dementia. Ann Neurol. 2008;64(1): 97–108Lancaster E, Dalmau J. Neuronal autoantigens-pathogenesis, associated disorders, and antibody testing; 2012.Frost B, Diamond MI. Prion-like mechanisms in neurodegenerative diseases. Nat Rev Neurosci. 2010;11(3): 155–9.Ganor Y, Goldberg-Stern H, Amrom D, Lerman-Sagie T, Teichberg VI, Pelled D, et al. Autoimmune epilepsy: some epilepsy patients harbor autoantibodies to glutamate receptors and dsDNA on both sides of the bloodbrain barrier, which may kill neurons and decrease in brain fluids after hemispherotomy. Clin Dev Immunol. 2004 Sep–Dec;11(3–4):241–52.Brenner T, Sills GJ, Hart Y, Howell S, Waters P, Brodie MJ, et al. Prevalence of neurologic autoantibodies in cohorts of patients with new and established epilepsy. Epilepsia. 2013 Jun;54(6):1028–35Prado CAC, Gallego AC. Autoimmune epilepsy—a new goal of science: report two cases in the San Jose Hospital, Bogota, Colombia. J Neurol Stroke. 2019;9(3):129–32.Kim MO, Geschwind MD. Clinical update of Jakob-Creutzfeldt disease. Curr Opin Neurol. 2015;28(3):302–10.Munné Díaz C, Grau Solà M, Torreño Sánchez M. Enfermedad de Creutzfeldt-jacob. Rev Científica la Soc Española Enfermería Neurológica [Internet]. Medicina en español. 2013 Jan 1 [cited 2020 Aug 27];37(1):29–32.Sanchez-Juan P, Green A, Ladogana A, Cuadrado-Corrales N, Sáanchez-Valle R, Mitrováa E, et al. CSF tests in the differential diagnosis of Creutzfeldt-Jakob disease. Neurology. 2006 Aug 22;67(4):637–43.Collins SJ, Sanchez-Juan P, Masters CL, Klug GM, van Duijn C, Poleggi A, et al. Determinants of diagnostic investigation sensitivities across the clinical spectrum of sporadic Creutzfeldt-Jakob disease. Brain. 2006 Sep; 129(Pt 9):2278–87. Epub 2006 Jul 1.Puoti G, Bizzi A, Forloni G, Safar JG, Tagliavini F, Gambetti P. Sporadic human prion diseases: molecular insights and diagnosis. Lancet Neurol. 2012;11(7):618–28.Zerr I, Pocchiari M, Collins S, Brandel JP, de Pedro Cuesta J, Knight RS, et al. Analysis of EEG and CSF 14-3-3 proteins as aids to the diagnosis of Creutzfeldt-Jakob disease. Neurology. 2000;55(6):811–5.van Sonderen A, Thijs RD, Coenders EC, Jiskoot LC, Sanchez E, de Bruijn MA, et al. Anti-LGI1 encephalitis: clinical syndrome and long-term follow-up. Neurology. 2016 Oct 4;87(14):1449–56. Epub 2016 Sep 2.Irani SR, Michell AW, Lang B, Pettingill P, Waters P, Johnson MR, et al. Faciobrachial dystonic seizures precede Lgi1 antibody limbic encephalitis. Ann Neurol. 2011 May;69(5):892–900. Epub 2011 Mar 17.Ekizoglu E, Tuzun E, Woodhall M, Lang B, Jacobson L, Icoz S, et al. Investigation of neuronal autoantibodies in two different focal epilepsy syndromes. Epilepsia. 2014;55(3):414–22Liimatainen S, Peltola J, Hietaharju A, Sabater L, Lang B. Lack of antibodies to NMDAR or VGKC-complex in GAD and cardiolipin antibody-positive refractory epilepsy. Epilepsy Res. 2014 Mar;108(3):592–6. Epub 2014 Jan 6.Lai M, Huijbers MG, Lancaster E, Graus F, Bataller L, Balice-Gordon R, et al. Investigation of LGI1 as the antigen in limbic encephalitis previously attributed to potassium channels: a case series. Lancet Neurol. 2010;9:776–85.Lancaster E, Huijbers MG, Bar V, Boronat A, Wong A, Martinez-Hernandez E, et al. Investigations of Caspr2, an autoantigen of encephalitis and neuromyotonia. Ann Neurol. 2011;69:303–11.Klein CJ, Lennon VA, Aston PA, McKeonO’Toole O, O’Toole A, Quek A, et al. Insights from LGI1 and CASPR2 potassium channel complex autoantibody subtyping. JAMA Neurol. 2013;70:229–34.Irani R, Alexander R, Waters P, Kleopa KA, Pettingill P, Zuliani L, et al. Antibodies to Kv1 potassium channelcomplex proteins leucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 in limbic encephalitis, Morvan’s syndrome and acquired neuromyotonia. Brain. 2010;133:2734–48.Montojo MT, Petit-Pedrol M, Graus F, Dalmau J. Clinical spectrum and diagnostic value of antibodies against the potassium channel related protein complex. Neurologia. 2015;30(5):295–301Fukata Y, Lovero KL, Iwanaga T, Watanabe A, Yokoi N, Tabuchi K, et al. Disruption of LGI1-linked synaptic complex causes abnormal synaptic transmission and epilepsy. Proc Natl Acad Sci U S A. 2010;107:3799–804.Yu YE, Wen L, Silva J, Li Z, Head K, Sossey-Alaoui K, et al. Lgi1 null mutant mice exhibit myoclonic seizures and CA1 neuronal hyperexcitability. Hum Mol Genet. 2010;19:1702–11.Titulaer MJ, McCracken L, Gabilondo I, Armangué T, Glaser C, Iizuka T, et al. 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Case Report: Three Case Reports of Rapidly Progressive Dementias and Narrative Review

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