Search

Your search keyword '"G. Moris de la Tassa"' showing total 9 results
Start Over Author "G. Moris de la Tassa"
9 results on '"G. Moris de la Tassa"'

1. Electrodiagnosis of Guillain-Barre syndrome in the International GBS Outcome Study: Differences in methods and reference values

Author

Samuel Arends, Judith Drenthen, Peter van den Bergh, Hessel Franssen, Robert D.M. Hadden, Badrul Islam, Satoshi Kuwabara, Ricardo C. Reisin, Nortina Shahrizaila, Hiroshi Amino, Giovanni Antonini, Shahram Attarian, Claudia Balducci, Fabio Barroso, Tulio Bertorini, Davide Binda, Thomas H. Brannagan, Jan Buermann, Carlos Casasnovas, Guido Cavaletti, Chi-Chao Chao, Mazen M. Dimachkie, Ernesto A. Fulgenzi, Giuliana Galassi, Gerardo Gutiérrez Gutiérrez, Thomas Harbo, Hans-Peter Hartung, Sung-Tsang Hsieh, Lynette Kiers, Helmar C. Lehmann, Fiore Manganelli, Girolama A. Marfia, Giorgia Mataluni, Julio Pardo, Yann Péréon, Yusuf A. Rajabally, Lucio Santoro, Yukari Sekiguchi, Beth Stein, Mark Stettner, Antonino Uncini, Christine Verboon, Camiel Verhamme, Michal Vytopil, Waqar Waheed, Min Wang, Sasha Zivkovic, Bart C. Jacobs, David R. Cornblath, J.M. Addington, S. Ajroud-Driss, H. Andersen, G. Antonini, S. Attarian, U.A. Badrising, G. Balloy, F.A. Barroso, K. Bateman, I.R. Bella, L. Benedetti, P. van den Bergh, T.E. Bertorini, R. Bhavaraju-Sanka, M. Bianco, T.H. Brannagan, C. Briani, null Buerrmann, M. Busby, S. Butterworth, C. Casasnovas, G. Cavaletti, C.C. Chao, G. Chavada, S. Chen, K.G. Claeys, M.E. Conti, D.R. Cornblath, J.S. Cosgrove, M.C. Dalakas, P. van Damme, E. Dardiotis, A. Davidson, M.A. Derejko, G.W. van Dijk, M.M. Dimachkie, P.A. van Doorn, C. Dornonville de la Cour, A. Echaniz-Laguna, F. Eftimov, C.G. Faber, R. Fazio, T.E. Feasby, C. Fokke, T. Fujioka, E.A. Fulgenzi, G. Galassi, T. Garcia-Sobrino, M.P.J. Garssen, C.J. Gijsbers, J.M. Gilchrist, H.J. Gilhuis, J.M. Goldstein, K.C. Gorson, N.A. Goyal, V. Granit, S.T.E. Grisanti, null Gutiérrez-Gutiérrez, L. Gutmann, R.D.M. Hadden, T. Harbo, H.P. Hartung, J.V. Holbech, J.K.L. Holt, S.T. Hsieh, M. Htut, R.A.C. Hughes, I. Illa, B. Islam, Z. Islam, B.C. Jacobs, J. Fehmi, K. Jellema, I. Jerico Pascual, K. Kaida, S. Karafiath, H.D. Katzberg, M.A. Khoshnoodi, L. Kiers, K. Kimpinski, R.P. Kleyweg, N. Kokubun, N.A. Kolb, R. van Koningsveld, A.J. van der Kooi, J.C.H.M. Kramers, K. Kuitwaard, S. Kusunoki, S. Kuwabara, J.Y. Kwan, S.S. Ladha, L. Landschoff Lassen, V. Lawson, H.C. Lehmann, E. Lee Pan, M.P.T. Lunn, H. Manji, G.A. Marfia, C. Márquez Infante, L. Martin-Aguilar, E. Martinez Hernandez, G. Mataluni, M. Mattiazi, C.J. McDermott, G.D. Meekins, J.A.L. Miller, Q.D. Mohammad, M.S. Monges, G. Moris de la Tassa, C. Nascimbene, F.J. Navacerrada-Barrero, E. Nobile-Orazio, R.J. Nowak, P.J. Orizaola, M. Osei-Bonsu, A.M. Pardal, J. Pardo, R.M. Pascuzzi, Y. Péréon, M.T. Pulley, L. Querol, S.W. Reddel, T. van der Ree, R.C. Reisin, S. Rinaldi, R.C. Roberts, I. Rojas-Marcos, null Rudnicki, G.M. Sachs, J.P.A. Samijn, L. Santoro, A. Schenone, M.J. Sedano Tous, N. Shahrizaila, K.A. Sheikh, N.J. Silvestri, S.H. Sindrup, C.L. Sommer, B. Stein, Y. Song, A.M. Stino, H. Tankisi, M.R. Tannemaat, P. Twydell, P.V. Vélez-Santamaria, J.D. Varrato, F.H. Vermeij, L.H. Visser, M.V. Vytopil, W. Waheed, C. Walgaard, Y.Z. Wang, H.J. Willison, P.W. Wirtz, Y. Yamagishi, L. Zhou, S.A. Zivkovic, Neurology, ANS - Neuroinfection & -inflammation, EURO-NMD, Immunology, Arends, S., Drenthen, J., van den Bergh, P., Franssen, H., Hadden, R. D. M., Islam, B., Kuwabara, S., Reisin, R. C., Shahrizaila, N., Amino, H., Antonini, G., Attarian, S., Balducci, C., Barroso, F., Bertorini, T., Binda, D., Brannagan, T. H., Buermann, J., Casasnovas, C., Cavaletti, G., Chao, C. -C., Dimachkie, M. M., Fulgenzi, E. A., Galassi, G., Gutierrez Gutierrez, G., Harbo, T., Hartung, H. -P., Hsieh, S. -T., Kiers, L., Lehmann, H. C., Manganelli, F., Marfia, G. A., Mataluni, G., Pardo, J., Pereon, Y., Rajabally, Y. A., Santoro, L., Sekiguchi, Y., Stein, B., Stettner, M., Uncini, A., Verboon, C., Verhamme, C., Vytopil, M., Waheed, W., Wang, M., Zivkovic, S., Jacobs, B. C., Cornblath, D. R., Arends, S, Drenthen, J, van den Bergh, P, Franssen, H, Hadden, R, Islam, B, Kuwabara, S, Reisin, R, Shahrizaila, N, Amino, H, Antonini, G, Attarian, S, Balducci, C, Barroso, F, Bertorini, T, Binda, D, Brannagan, T, Buermann, J, Casasnovas, C, Cavaletti, G, Chao, C, Dimachkie, M, Fulgenzi, E, Galassi, G, Gutierrez Gutierrez, G, Harbo, T, Hartung, H, Hsieh, S, Kiers, L, Lehmann, H, Manganelli, F, Marfia, G, Mataluni, G, Pardo, J, Pereon, Y, Rajabally, Y, Santoro, L, Sekiguchi, Y, Stein, B, Stettner, M, Uncini, A, Verboon, C, Verhamme, C, Vytopil, M, Waheed, W, Wang, M, Zivkovic, S, Jacobs, B, Cornblath, D, UCL - (SLuc) Centre de référence neuromusculaire, and UCL - (SLuc) Service de neurologie

Subjects
Nerve conduction studie, Electrodiagnòstic, Malalties autoimmunitàries, Electromyography, Electrodiagnosis, Autoimmune diseases, Neural Conduction, Medizin, Settore MED/26, Guillain-Barre Syndrome, AIDP, AMSAN, Sensory Systems, Reference values, Clinical trials, AMAN, Neurology, Physiology (medical), Outcome Assessment, Health Care, Humans, Nerve conduction studies, Neurology (clinical), Reference value, Assaigs clínics
Abstract

Objective: To describe the heterogeneity of electrodiagnostic (EDx) studies in Guillain-Barre syndrome (GBS) patients collected as part of the International GBS Outcome Study (IGOS). Methods: Prospectively collected clinical and EDx data were available in 957 IGOS patients from 115 centers. Only the first EDx study was included in the current analysis. Results: Median timing of the EDx study was 7 days (interquartile range 4-11) from symptom onset. Methodology varied between centers, countries and regions. Reference values from the responding 103 centers were derived locally in 49%, from publications in 37% and from a combination of these in the remaining 15%. Amplitude measurement in the EDx studies (baseline-to-peak or peak-to-peak) differed from the way this was done in the reference values, in 22% of motor and 39% of sensory conduction. There was marked variability in both motor and sensory reference values, although only a few outliers accounted for this. Conclusions: Our study showed extensive variation in the clinical practice of EDx in GBS patients among IGOS centers across the regions. Significance: Besides EDx variation in GBS patients participating in IGOS, this diversity is likely to be present in other neuromuscular disorders and centers. This underlines the need for standardization of EDx in future multinational GBS studies.(c) 2022 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Published
2022
Full Text
View/download PDF

2. 20666. MIASTENIA-MIOSITIS ASOCIADA A INHIBIDORES DE PUNTOS DE CONTROL INMUNITARIO: ANÁLISIS RETROSPECTIVO MULTICÉNTRICO EN ESPAÑA

Author

R. Velasco Fargas, J. Cabrera Maqueda, C. Marco Cazcarra, E. Fonseca, J. Chico García, F. Gómez Fernández, L. del Pino Tejado, J. Cabello Murgui, R. Caldú, C. Fadrique, C. Sánchez Vizcaíno, H. Hernández Tost, M. Ros, J. Gállego Pérez- Larraya, C. Jauregui Larrañaga, M. García Yepes, A. Chavarría Miranda, C. González Mingot, G. Morís de la Tassa, M. Alañá García, L. Torné Hernández, A. Macías Gómez, J. Pouso Diz, S. Besora Tavera, P. Cabezudo García, C. Izquierdo Gracia, A. Boix Lago, A. Carvajal Hernández, J. Álvarez Troncoso, M. Barón Rubio, J. Riancho, M. Simó Parra, and E. Martínez Hernández

Subjects
Neurology. Diseases of the nervous system, RC346-429
Published
2024
Full Text
View/download PDF

5. Autoantibody screening in Guillain-Barre syndrome

Author

T. Franco, Laura Martínez-Martínez, Christian Homedes, Cristina Domínguez-González, Elba Pascual-Goñi, Ricardo Rojas-García, José Berciano, Elena Cortés-Vicente, Julio Pardo-Fernández, Joana Turón, I. Rojas-Marcos, M. J. Sedano Tous, Cándido Juárez, Eugenia Martinez-Hernandez, Ivonne Jericó-Pascual, Luis Querol, María Concepción Jimeno-Montero, J. Diaz-Manera, Isabel Illa, C. Lleixa, Xavier Suárez-Calvet, M. Caballero, G. Moris de la Tassa, Celedonio Márquez-Infante, Gerardo Gutiérrez-Gutiérrez, N. De Luna, Tania García-Sobrino, Lorena Martín-Aguilar, Carlos Casasnovas, and Eduard Gallardo

Subjects
Neurons, Anti-ganglioside, biology, Guillain-Barre syndrome, business.industry, Serum autoantibodies, Autoantibody, medicine.disease, Prognosis, Pathogenesis, Antigen, Peripheral nerve, Nerve cells, Immunology, biology.protein, Guillain-Barre syndrome (GBS), Medicine, Antibody, business, Autoantibodies
Abstract

Background Guillain-Barre syndrome (GBS) is an acute inflammatory neuropathy with a heterogeneous presentation. Although some evidences support the role of autoantibodies in its pathogenesis, the target antigens remain unknown in a substantial proportion of GBS patients. The objective of this study is to screen for autoantibodies targeting peripheral nerve components in Guillain-Barre syndrome. Methods Autoantibody screening was performed in serum samples from all GBS patients included in the International GBS Outcome study by 11 different Spanish centres. The screening included testing for anti-ganglioside antibodies, anti-nodo/paranodal antibodies, immunocytochemistry on neuroblastoma-derived human motor neurons and murine dorsal root ganglia (DRG) neurons, and immunohistochemistry on monkey peripheral nerve sections. We analysed the staining patterns of patients and controls. The prognostic value of anti-ganglioside antibodies was also analysed. Results None of the GBS patients (n = 100) reacted against the nodo/paranodal proteins tested, and 61 (61%) were positive for, at least, one anti-ganglioside antibody. GBS sera reacted strongly against DRG neurons more frequently than controls both with IgG (6% vs 0%; p = 0.03) and IgM (11% vs 2.2%; p = 0.02) immunodetection. No differences were observed in the proportion of patients reacting against neuroblastoma-derived human motor neurons. Reactivity against monkey nerve tissue was frequently detected both in patients and controls, but specific patterns were only detected in GBS patients: IgG from 13 (13%) patients reacted strongly against Schwann cells. Finally, we confirmed that IgG anti-GM1 antibodies are associated with poorer outcomes independently of other known prognostic factors. Conclusion Our study confirms that (1) GBS patients display a heterogeneous repertoire of autoantibodies targeting nerve cells and structures; (2) gangliosides are the most frequent antigens in GBS patients and have a prognostic value; (3) further antigen-discovery experiments may elucidate other potential antigens in GBS.

Published
2021

6. Clinical guide for the diagnosis and follow-up of myotonic dystrophy type 1, MD1 or Steinert's disease

Author

G. Gutiérrez Gutiérrez, J. Díaz-Manera, M. Almendrote, S. Azriel, J. Eulalio Bárcena, P. Cabezudo García, A. Camacho Salas, C. Casanova Rodríguez, A.M. Cobo, P. Díaz Guardiola, R. Fernández-Torrón, M.P. Gallano Petit, P. García Pavía, M. Gómez Gallego, A.J. Gutiérrez Martínez, I. Jericó, S. Kapetanovic García, A. López de Munaín Arregui, L. Martorell, G. Morís de la Tassa, R. Moreno Zabaleta, J.L. Muñoz-Blanco, J. Olivar Roldán, S.I. Pascual Pascual, R. Peinado Peinado, H. Pérez, J.J. Poza Aldea, M. Rabasa, A. Ramos, A. Rosado Bartolomé, M.Á. Rubio Pérez, J.A. Urtizberea, G. Zapata-Wainberg, and E. Gutiérrez-Rivas

Subjects
Guía clínica, Enfermedad de Steinert, Distrofia miotónica tipo 1, Complicaciones, Recomendaciones, Disfagia, Neurology. Diseases of the nervous system, RC346-429
Abstract

Background and objectives: Steinert's disease or myotonic dystrophy type 1 (MD1), (OMIM 160900), is the most prevalent myopathy in adults. It is a multisystemic disorder with dysfunction of virtually all organs and tissues and a great phenotypical variability, which implies that it has to be addressed by different specialities with experience in the disease. The knowledge of the disease and its management has changed dramatically in recent years. This guide tries to establish recommendations for the diagnosis, prognosis, follow-up and treatment of the complications of MD1. Material and methods: Consensus guide developed through a multidisciplinary approach with a systematic literature review. Neurologists, pulmonologists, cardiologists, endocrinologists, neuropaediatricians and geneticists have participated in the guide. Recommendations: The genetic diagnosis should quantify the number of CTG repetitions. MD1 patients need cardiac and respiratory lifetime follow-up. Before any surgery under general anaesthesia, a respiratory evaluation must be done. Dysphagia must be screened periodically. Genetic counselling must be offered to patients and relatives. Conclusion: MD1 is a multisystemic disease that requires specialised multidisciplinary follow-up. Resumen: Antecedentes y objetivos: La enfermedad de Steinert o distrofia miotónica tipo 1 (DM1), (OMIM 160900) es la miopatía más prevalente en el adulto. Es una enfermedad multisistémica con alteración de prácticamente todos los órganos y tejidos y una variabilidad fenotípica muy amplia, lo que implica que deba ser atendida por diferentes especialistas que dominen las alteraciones más importantes. En los últimos años se ha avanzado de manera exponencial en el conocimiento de la enfermedad y en su manejo. El objetivo de la guía es establecer recomendaciones para el diagnóstico, el pronóstico, el seguimiento y el tratamiento de las diferentes alteraciones de la DM1. Material y métodos: Esta guía de consenso se ha realizado de manera multidisciplinar. Se ha contado con neurólogos, neumólogos, cardiólogos, endocrinólogos, neuropediatras y genetistas que han realizado una revisión sistemática de la literatura. Recomendaciones: Se recomienda realizar un diagnóstico genético con cuantificación precisa de tripletes CTG. Los pacientes con DM1 deben seguir control cardiológico y neumológico de por vida. Antes de cualquier cirugía con anestesia general debe realizarse una evaluación respiratoria. Debe monitorizarse la presencia de síntomas de disfagia periódicamente. Debe ofrecerse consejo genético a los pacientes con DM1 y a sus familiares. Conclusión: La DM1 es una enfermedad multisistémica que requiere un seguimiento en unidades especializadas multidisciplinares.

Published
2020
Full Text
View/download PDF

7. Guía clínica para el diagnóstico y seguimiento de la distrofia miotónica tipo 1, DM1 o enfermedad de Steinert

Author

G. Gutiérrez Gutiérrez, J. Díaz-Manera, M. Almendrote, S. Azriel, J. Eulalio Bárcena, P. Cabezudo García, A. Camacho Salas, C. Casanova Rodríguez, A.M. Cobo, P. Díaz Guardiola, R. Fernández-Torrón, M.P. Gallano Petit, P. García Pavía, M. Gómez Gallego, A.J. Gutiérrez Martínez, I. Jericó, S. Kapetanovic García, A. López de Munaín Arregui, L. Martorell, G. Morís de la Tassa, R. Moreno Zabaleta, J.L. Muñoz-Blanco, J. Olivar Roldán, S.I. Pascual Pascual, R. Peinado Peinado, H. Pérez, J.J. Poza Aldea, M. Rabasa, A. Ramos, A. Rosado Bartolomé, M.Á. Rubio Pérez, J.A. Urtizberea, G. Zapata-Wainberg, and E. Gutiérrez-Rivas

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Resumen: Antecedentes y objetivos: La enfermedad de Steinert o distrofia miotónica tipo 1 (DM1), (OMIM 160900) es la miopatía más prevalente en el adulto. Es una enfermedad multisistémica con alteración de prácticamente todos los órganos y tejidos y una variabilidad fenotípica muy amplia, lo que implica que deba ser atendida por diferentes especialistas que dominen las alteraciones más importantes. En los últimos años se ha avanzado de manera exponencial en el conocimiento de la enfermedad y en su manejo. El objetivo de la guía es establecer recomendaciones para el diagnóstico, el pronóstico, el seguimiento y el tratamiento de las diferentes alteraciones de la DM1. Material y métodos: Esta guía de consenso se ha realizado de manera multidisciplinar. Se ha contado con neurólogos, neumólogos, cardiólogos, endocrinólogos, neuropediatras y genetistas que han realizado una revisión sistemática de la literatura. Recomendaciones: Se recomienda realizar un diagnóstico genético con cuantificación precisa de tripletes CTG. Los pacientes con DM1 deben seguir control cardiológico y neumológico de por vida. Antes de cualquier cirugía con anestesia general debe realizarse una evaluación respiratoria. Debe monitorizarse la presencia de síntomas de disfagia periódicamente. Debe ofrecerse consejo genético a los pacientes con DM1 y a sus familiares. Conclusión: La DM1 es una enfermedad multisistémica que requiere un seguimiento en unidades especializadas multidisciplinares. Abstract: Background and objectives: Steinert's disease or myotonic dystrophy type 1 (MD1), (OMIM 160900), is the most prevalent myopathy in adults. It is a multisystemic disorder with dysfunction of virtually all organs and tissues and a great phenotypical variability, which implies that it has to be addressed by different specialities with experience in the disease. The knowledge of the disease and its management has changed dramatically in recent years. This guide tries to establish recommendations for the diagnosis, prognosis, follow-up and treatment of the complications of MD1. Material and methods: Consensus guide developed through a multidisciplinary approach with a systematic literature review. Neurologists, pulmonologists, cardiologists, endocrinologists, neuropaediatricians and geneticists have participated in the guide. Recommendations: The genetic diagnosis should quantify the number of CTG repetitions. MD1 patients need cardiac and respiratory lifetime follow-up. Before any surgery under general anaesthesia, a respiratory evaluation must be done. Dysphagia must be screened periodically. Genetic counselling must be offered to patients and relatives. Conclusion: MD1 is a multisystemic disease that requires specialised multidisciplinary follow-up. Palabras clave: Guía clínica, Enfermedad de Steinert, Distrofia miotónica tipo 1, Complicaciones, Recomendaciones, Disfagia, Keywords: Clinical guideline, Steinert's disease, Myotonic dystrophy type 1, Complications, Recommendations, Dysphagia

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results