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4. Rare deletions at 16p13.11 predispose to a diverse spectrum of sporadic epilepsy syndromes

Author

Heinzen, Erin L., Radtke, Rodney A., Urban, Thomas J., Cavalleri, Gianpiero L., Depondt, Chantal, Need, Anna C., Walley, Nicole M., Nicoletti, Paola, Dongliang Ge, Catarino, Claudia B., Duncan, John S., Kasperaviciute, Dalia, Tate, Sarah K., Caboclo, Luis O.mSander, Josemir W., Clayton, Lisa, Linney, Kristen N., Shianna, Kevin V., Gumbs, Curtis E., Smith, Jason, Cronin, Kenneth D., Maia, Jessica M., Doherty, Colin P., Pandolfo, Massimo, Leppert, David, Middleton, Lefkos T., Gibson, Rachel A., Johnson, Michael R., Matthews, Paul M., Hosford, David, Kalviainen, Reetta, Eriksson, Kai, Kantanen, Anne-Mari, Dorn, Thomas; Hansen, Jorg, Kramer, Gunter, Steinhoff, Bernhard J., Wieser, Heinz-Gregor, Zumsteg, Dominik, Ortega, Marcos, Wood, Nicholas W., Huxley-Jones, Juli, Mikati, Mohamad, Gallentine, William B., Husain, Aatif M., Buckley, Patrick G., Stallings, Ray L., Podgoreanu, Mihai V., Delanty, Norman, Sisodiya, Sanjay M., and Goldstein, David B.

Subjects
Chromosome deletion -- Research, Epilepsy -- Genetic aspects, Epilepsy -- Care and treatment, Gene expression -- Analysis, Biological sciences
Abstract

Genome-wide screens were used to identify copy number variation in 3812 patients with a diverse spectrum of epilepsy syndromes and in 1299 neurologically-normal controls to evaluate the role of 16p13.11 deletions and other structural variation in epilepsy disorders. The data implicated 16p13.11 and possibly other large deletions as risk factors for a wide range of epilepsy disorders and appear to point toward haploinsufficiency as a contributor to the pathogenicity of deletions.

Published
2010

5. Epilepsy, hippocampal sclerosis and febrile seizures linked by common genetic variation around SCN1A

Author

Kasperavičiūtė, Dalia, Catarino, Claudia B., Matarin, Mar, Leu, Costin, Novy, Jan, Tostevin, Anna, Leal, Bárbara, Hessel, Ellen V. S., Hallmann, Kerstin, Hildebrand, Michael S., Dahl, Hans-Henrik M., Ryten, Mina, Trabzuni, Daniah, Ramasamy, Adaikalavan, Alhusaini, Saud, Doherty, Colin P., Dorn, Thomas, Hansen, Jörg, Krämer, Günter, Steinhoff, Bernhard J., Zumsteg, Dominik, Duncan, Susan, Kälviäinen, Reetta K., Eriksson, Kai J., Kantanen, Anne-Mari, Pandolfo, Massimo, Gruber-Sedlmayr, Ursula, Schlachter, Kurt, Reinthaler, Eva M., Stogmann, Elisabeth, Zimprich, Fritz, Théâtre, Emilie, Smith, Colin, O’Brien, Terence J., Meng Tan, K., Petrovski, Slave, Robbiano, Angela, Paravidino, Roberta, Zara, Federico, Striano, Pasquale, Sperling, Michael R., Buono, Russell J., Hakonarson, Hakon, Chaves, João, Costa, Paulo P., Silva, Berta M., da Silva, António M., de Graan, Pierre N. E., Koeleman, Bobby P. C., Becker, Albert, Schoch, Susanne, von Lehe, Marec, Reif, Philipp S., Rosenow, Felix, Becker, Felicitas, Weber, Yvonne, Lerche, Holger, Rössler, Karl, Buchfelder, Michael, Hamer, Hajo M., Kobow, Katja, Coras, Roland, Blumcke, Ingmar, Scheffer, Ingrid E., Berkovic, Samuel F., Weale, Michael E., Delanty, Norman, Depondt, Chantal, Cavalleri, Gianpiero L., Kunz, Wolfram S., and Sisodiya, Sanjay M.

Published
2013
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11. Common genetic variation and susceptibility to partial epilepsies: a genome-wide association study

Author

Kasperavičiūtė, Dalia, Catarino, Claudia B., Heinzen, Erin L., Depondt, Chantal, Cavalleri, Gianpiero L., Caboclo, Luis O., Tate, Sarah K., Jamnadas-Khoda, Jenny, Chinthapalli, Krishna, Clayton, Lisa M.S., Shianna, Kevin V., Radtke, Rodney A., Mikati, Mohamad A., Gallentine, William B., Husain, Aatif M., Alhusaini, Saud, Leppert, David, Middleton, Lefkos T., Gibson, Rachel A., Johnson, Michael R., Matthews, Paul M., Hosford, David, Heuser, Kjell, Amos, Leslie, Ortega, Marcos, Zumsteg, Dominik, Wieser, Heinz-Gregor, Steinhoff, Bernhard J., Krämer, Günter, Hansen, Jörg, Dorn, Thomas, Kantanen, Anne-Mari, Gjerstad, Leif, Peuralinna, Terhi, Hernandez, Dena G., Eriksson, Kai J., Kälviäinen, Reetta K., Doherty, Colin P., Wood, Nicholas W., Pandolfo, Massimo, Duncan, John S., Sander, Josemir W., Delanty, Norman, Goldstein, David B., and Sisodiya, Sanjay M.

Published
2010
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21. Correspondence

Author

Zumsteg, Dominik and Wennberg, Richard

Published
2017

23. Antibody-Mediated Status Epilepticus: A Retrospective Multicenter Survey

Author

Holzer, Franz Josef, primary, Rossetti, Andrea O., additional, Heritier-Barras, Anne-Chantal, additional, Zumsteg, Dominik, additional, Roebling, Robert, additional, Huber, Roman, additional, Lerche, Holger, additional, Kiphuth, Ines C., additional, Bardutzky, Jürgen, additional, Bien, Christian G., additional, Tröger, Mathias, additional, Schoch, Gaby, additional, Prüss, Harald, additional, and Seeck, Margitta, additional

Published
2012
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33. Propagation of interictal discharges in temporal lobe epilepsy: Correlation of spatiotemporal mapping with intracranial foramen ovale electrode recordings

Author

Zumsteg, Dominik, Friedman, Alon, Wieser, Heinz Gregor, and Wennberg, Richard A.

Subjects
*TEMPORAL lobe epilepsy, *EPILEPSY, *TOMOGRAPHY, *ELECTRODES, *TEMPORAL lobe
Abstract

Abstract: Objective: We have investigated intracerebral propagation of interictal epileptiform discharges (IED) in patients with mesial temporal lobe epilepsy (MTLE) by using spatiotemporal source maps based on statistical nonparametric mapping (SNPM) of low resolution electromagnetic tomography (LORETA) values. Methods: We analyzed 30 patterns of IED recorded simultaneously with scalp and intracranial foramen ovale (FO) electrodes in 15 consecutive patients with intractable MTLE. The scalp EEG signals were averaged time-locked to the peak activity in bilateral 10-contact FO electrode recordings. SNPM was applied to LORETA values and spatiotemporal source maps were created by allocating the t-values over time to their corresponding Brodmann areas. Propagation was defined as secondary statistically significant involvement of distinct cortical areas separated by >15ms. The results were correlated with intracranial data obtained from FO electrode recordings and with scalp EEG recordings. All patients underwent subsequent amygdalo-hippocampectomy and outcome was assessed one year after surgery. Results: We found mesial to lateral propagation in 6/30 IED patterns (20%, four patients), lateral to mesial propagation in 4/30 IED patterns (13.3%, four patients) and simultaneous (within 15ms) activation of mesial and lateral temporal areas in 6/30 IED patterns (20%, five patients). Propagation generally occurred within 30ms and was always limited to ipsilateral cortical regions. Nine/30 IED patterns (30%) showed restricted activation of mesial temporal structures and no significant solutions were found in 5/30 IED patterns (16.7%). There was no clear association between the number or characteristics of IED patterns and the postsurgical outcome. Conclusions: Spatiotemporal mapping of SNPM LORETA accurately describes mesial to lateral temporal propagation of IED, and vice versa, which commonly occur in patients with MTLE. Significance: Intracerebral propagation must be considered when using non-invasive source algorithms in patients with MTLE. Spatiotemporal mapping might be useful for visualizing this propagation. [Copyright &y& Elsevier]

Published
2006
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34. A model for foramen ovale puncture training: technical note.

Author

Wieser, Heinz Gregor and Zumsteg, Dominik

Subjects
*LETTERS to the editor, *SURGERY
Abstract

A letter to the editor is presented in response to the article "A model for foramen ovale puncture training: technical note," by D. B. Almeida and his collaborators in the previous issue.

Published
2006
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37. Whiplash and Concussion: Similar Acute Changes in Middle-Latency SEPs

Author

Dominik Zumsteg, Eva Gütling, Richard A. Wennberg, Klaus Hess, University of Zurich, and Zumsteg, Dominik

Subjects
Gynecology, medicine.medical_specialty, Injury control, Accident prevention, business.industry, Middle latency, Poison control, General Medicine, 142-005 142-005, 03 medical and health sciences, 2728 Neurology (clinical), 0302 clinical medicine, Neurology, 2808 Neurology, medicine, 030212 general & internal medicine, Neurology (clinical), business, human activities, 030217 neurology & neurosurgery
Abstract

Objectif: Les potentiels evoques somesthesiques (PESs) de latence moyenne obtenus par stimulation du nerf median constituent une mesure sensible de la fonction corticale. Le but de cette etude etait de determiner si les forces mecaniques impliquees dans le coup de fouet cervical et dans la commotion cerebrale alterent le traitement normal des PESs de latence moyenne. Methodes : Il s'agit d'une etude pilote transversale au cours de laquelle nous avons evalue 20 sujets qui avaient subi un coup de fouet cervical. La moitie des sujets ont ete evalues entre 0,5 a 2 mois apres l'incident et l'autre moitie de 6 a 41 mois apres. Nous les avons compares a 83 sujets temoins en sante au moyen de la technique standard d'evaluation des PESs de latence moyenne. Au cours d'une etude prospective subsequente, nous avons evalue des sujets presentant soit un coup de fouet cervical aigu (n = 13) ou une commotion cerebrale de grade 3 (n = 16) dans les 48 heures de l'incident et 3 mois apres. Resultats : Dans l'etude pilote, la composante de latence moyenne N60 etait significativement augmentee chez les dix sujets evalues dans les deux premiers mois apres l'incident. Par contre, les dix sujets examines plus de six mois apres l'incident avaient des latences normales. Dans l'etude prospective, les latences N60 etaient augmentees apres le coup de fouet cervical et la commotion cerebrale lors de l'evaluation faite dans les 48 heures de l'incident. Apres trois mois, les latences etaient ameliorees chez les sujets ayant subi un coup de fouet cervical ou une commotion cerebrale, meme si elles demeuraient significativement differentes de celles des temoins. Conclusions : Le coup de fouet cervical et la commotion cerebrale modifient le traitement de la composante N60 des PESs de latence moyenne au cours de la periode post-traumatique aigue. Les changements aigus semblent se normaliser entre trois et six mois apres la blessure. La similitude des PESs suggere que le chevauchement de la symptomatologie clinique apres le coup de fouet cervical et apres la commotion cerebrale puisse refleter un mecanisme sous-jacent similaire soit une legere lesion cerebrale traumatique rotatoire.

Published
2017

39. TGF-beta receptor-mediated albumin uptake into astrocytes is involved in neocortical epileptogenesis.

Author

Ivens S, Kaufer D, Flores LP, Bechmann I, Zumsteg D, Tomkins O, Seiffert E, Heinemann U, and Friedman A

Subjects
Animals, Blood-Brain Barrier physiopathology, Disease Models, Animal, Down-Regulation, Electroencephalography, Epilepsy chemically induced, Epilepsy metabolism, Magnetic Resonance Imaging, Neocortex drug effects, Neocortex metabolism, Neurons physiology, Potassium metabolism, Potassium Channels, Inwardly Rectifying metabolism, Rats, Rats, Wistar, Serum Albumin toxicity, Tissue Culture Techniques, Astrocytes metabolism, Epilepsy physiopathology, Neocortex physiopathology, Receptors, Transforming Growth Factor beta physiology, Serum Albumin pharmacokinetics
Abstract

It has long been recognized that insults to the cerebral cortex, such as trauma, ischaemia or infections, may result in the development of epilepsy, one of the most common neurological disorders. Human and animal studies have suggested that perturbations in neurovascular integrity and breakdown of the blood-brain barrier (BBB) lead to neuronal hypersynchronization and epileptiform activity, but the mechanisms underlying these processes are not known. In this study, we reveal a novel mechanism for epileptogenesis in the injured brain. We used focal neocortical, long-lasting BBB disruption or direct exposure to serum albumin in rats (51 and 13 animals, respectively, and 26 controls) as well as albumin exposure in brain slices in vitro. Most treated slices (72%, n = 189) displayed hypersynchronous propagating epileptiform field potentials when examined 5-49 days after treatment, but only 14% (n = 71) of control slices showed similar responses. We demonstrate that direct brain exposure to serum albumin is associated with albumin uptake into astrocytes, which is mediated by transforming growth factor beta receptors (TGF-betaRs). This uptake is followed by down regulation of inward-rectifying potassium (Kir 4.1) channels in astrocytes, resulting in reduced buffering of extracellular potassium. This, in turn, leads to activity-dependent increased accumulation of extracellular potassium, resulting in facilitated N-methyl-d-aspartate-receptor-mediated neuronal hyperexcitability and eventually epileptiform activity. Blocking TGF-betaR in vivo reduces the likelihood of epileptogenesis in albumin-exposed brains to 29.3% (n = 41 slices, P < 0.05). We propose that the above-described cascade of events following common brain insults leads to brain dysfunction and eventually epilepsy and suggest TGF-betaRs as a possible therapeutic target.

Published
2007
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