T
Thomas V. Wuttke
Researcher at University of Tübingen
Publications - 34
Citations - 2513
Thomas V. Wuttke is an academic researcher from University of Tübingen. The author has contributed to research in topics: Epilepsy & Medicine. The author has an hindex of 18, co-authored 32 publications receiving 2175 citations. Previous affiliations of Thomas V. Wuttke include Harvard University & University of Southern Denmark.
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Journal ArticleDOI
GLUT1 mutations are a cause of paroxysmal exertion-induced dyskinesias and induce hemolytic anemia by a cation leak
Yvonne G. Weber,Alexander Storch,Thomas V. Wuttke,Knut Brockmann,Judith S. Kempfle,Snezana Maljevic,Lucia Margari,Christoph Kamm,Susanne A. Schneider,Stephan M. Huber,Arnulf Pekrun,Robert Roebling,Guiscard Seebohm,Saisudha Koka,Camelia Lang,Eduard Kraft,Dragica Blazevic,Alberto Salvo-Vargas,Michael Fauler,Felix M. Mottaghy,Alexander Münchau,Mark J. Edwards,Anna Presicci,Francesco Margari,Thomas Gasser,Florian Lang,Kailash P. Bhatia,Frank Lehmann-Horn,Holger Lerche +28 more
TL;DR: It is proposed that the dyskinesias result from an exertion-induced energy deficit that may cause episodic dysfunction of the basal ganglia, and that the hemolysis with echinocytosis may result from alterations in intracellular electrolytes caused by a cation leak through mutant GLUT1.
Journal ArticleDOI
Paroxysmal exercise-induced dyskinesia and epilepsy is due to mutations in SLC2A1, encoding the glucose transporter GLUT1.
Arvid Suls,Peter Dedeken,Karolien Goffin,Hilde Van Esch,Patrick Dupont,David Cassiman,Judith S. Kempfle,Thomas V. Wuttke,Yvonne G. Weber,Holger Lerche,Zaid Afawi,Wim Vandenberghe,Amos D. Korczyn,Samuel F. Berkovic,Dana Ekstein,Sara Kivity,Philippe Ryvlin,L Claes,Liesbet Deprez,Snezana Maljevic,Alberto Vargas,Tine Van Dyck,Dirk Goossens,Jurgen Del-Favero,Koen Van Laere,Peter De Jonghe,Wim Van Paesschen +26 more
TL;DR: In this article, the authors performed a clinical evaluation and genetic analysis in a five-generation family with co-occurrence of exercise-induced dyskinesia and epilepsy (n = 39), suggesting that this combination represents a clinical entity.
Journal Article
Paroxysmal exercise-induced dyskinesia and epilepsy due to mutations in SLC2A1, encoding the glucose transporter, Gluti
David Cassiman,A Suls,Peter Dedeken,Karolien Goffin,Hilde Van Esch,Patrick Dupont,Judith S. Kempfle,Thomas V. Wuttke,Yvonne G. Weber,Holger Lerche,Zaid Afawi,A. D Korezyn,Samuel F. Berkovic,Dana Ekstein,Sara Kivity,Philippe Ryvlin,L Claes,Liesbet Deprez,Snezana Maljevic,A Vargas,Tom Van Dyck,Dirk Goossens,Jurgen Del-Favero,Koen Van Laere,P. De Jonghe,Wim Van Paesschen +25 more
TL;DR: Co-occurring PED and epilepsy can be due to autosomal dominant heterozygous SLC2A1 mutations, expanding the phenotypic spectrum associated with GLUT1 deficiency and providing a potential new treatment option for this clinical syndrome.
Journal ArticleDOI
Early-onset absence epilepsy caused by mutations in the glucose transporter GLUT1.
Arvid Suls,Saul A. Mullen,Yvonne G. Weber,Kristien Verhaert,Berten Ceulemans,Renzo Guerrini,Thomas V. Wuttke,Alberto Salvo-Vargas,Liesbet Deprez,L Claes,Albena Jordanova,Samuel F. Berkovic,Holger Lerche,Peter De Jonghe,Ingrid E. Scheffer,Ingrid E. Scheffer +15 more
TL;DR: Findings suggest GLUT1 deficiency underlies a significant proportion of early‐onset absence epilepsy, which has both genetic counseling and treatment implications because the ketogenic diet is effective in GLut1 deficiency.
Journal ArticleDOI
The new anticonvulsant retigabine favors voltage-dependent opening of the Kv7.2 (KCNQ2) channel by binding to its activation gate.
TL;DR: In this article, a set of chimeras were constructed using the neuronal K v 7.2 (KCNQ2 ) channel, which is activated by retigabine, and the cardiac Kv 7.1 ( KCNQ1 ) channel which is not affected by this drug.