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1. Brivaracetam as add-on treatment in patients with post-stroke epilepsy: real-world data from the BRIVAracetam add-on First Italian netwoRk Study (BRIVAFIRST)

Author

Simona Lattanzi, Laura Canafoglia, Maria Paola Canevini, Sara Casciato, Emanuele Cerulli Irelli, Valentina Chiesa, Filippo Dainese, Giovanni De Maria, Giuseppe Didato, Giancarlo Di Gennaro, Giovanni Falcicchio, Martina Fanella, Edoardo Ferlazzo, Massimo Gangitano, Angela La Neve, Oriano Mecarelli, Elisa Montalenti, Alessandra Morano, Federico Piazza, Chiara Pizzanelli, Patrizia Pulitano, Federica Ranzato, Eleonora Rosati, Laura Tassi, Carlo Di Bonaventura, Angela Alicino, Michele Ascoli, Giovanni Assenza, Federica Avorio, Valeria Badioni, Paola Banfi, Emanuele Bartolini, Luca Manfredi Basili, Vincenzo Belcastro, Simone Beretta, Irene Berto, Martina Biggi, Giuseppe Billo, Giovanni Boero, Paolo Bonanni, Jole Bongorno, Francesco Brigo, Emanuele Caggia, Claudia Cagnetti, Carmen Calvello, Edward Cesnik, Gigliola Chianale, Domenico Ciampanelli, Roberta Ciuffini, Dario Cocito, Donato Colella, Margerita Contento, Cinzia Costa, Eduardo Cumbo, Alfredo D'Aniello, Francesco Deleo, Jacopo C DiFrancesco, Roberta Di Giacomo, Alessandra Di Liberto, Elisabetta Domina, Fedele Dono, Vania Durante, Maurizio Elia, Anna Estraneo, Giacomo Evangelista, Maria Teresa Faedda, Ylenia Failli, Elisa Fallica, Jinane Fattouch, Alessandra Ferrari, Florinda Ferreri, Giacomo Fisco, Davide Fonti, Francesco Fortunato, Nicoletta Foschi, Teresa Francavilla, Rosita Galli, Stefano Gazzina, Anna Teresa Giallonardo, Filippo Sean Giorgi, Loretta Giuliano, Francesco Habetswallner, Francesca Izzi, Benedetta Kassabian, Angelo Labate, Concetta Luisi, Matteo Magliani, Giulia Maira, Luisa Mari, Daniela Marino, Addolorata Mascia, Alessandra Mazzeo, Chiara Milano, Stefano Meletti, Annacarmen Nilo, Biagio Orlando, Francesco Paladin, Maria Grazia Pascarella, Chiara Pastori, Giada Pauletto, Alessia Peretti, Gabriella Perri, Marianna Pezzella, Marta Piccioli, Pietro Pignatta, Nicola Pilolli, Francesco Pisani, Laura Rosa Pisani, Fabio Placidi, Patrizia Pollicino, Vittoria Porcella, Silvia Pradella, Monica Puligheddu, Stefano Quadri, Pier Paolo Quarato, Rui Quintas, Rosaria Renna, Giada Ricciardo Rizzo, Adriana Rum, Enrico Michele Salamone, Ersilia Savastano, Maria Sessa, David Stokelj, Elena Tartara, Mario Tombini, Gemma Tumminelli, Anna Elisabetta Vaudano, Maria Ventura, Ilaria Viganò, Emanuela Viglietta, Aglaia Vignoli, Flavio Villani, Elena Zambrelli, Lelia Zummo, Lattanzi S., Canafoglia L., Canevini M.P., Casciato S., Cerulli Irelli E., Chiesa V., Dainese F., De Maria G., Didato G., Di Gennaro G., Falcicchio G., Fanella M., Ferlazzo E., Gangitano M., La Neve A., Mecarelli O., Montalenti E., Morano A., Piazza F., Pizzanelli C., Pulitano P., Ranzato F., Rosati E., Tassi L., Di Bonaventura C., Alicino A., Ascoli M., Assenza G., Avorio F., Badioni V., Banfi P., Bartolini E., Basili L.M., Belcastro V., Beretta S., Berto I., Biggi M., Billo G., Boero G., Bonanni P., Bongiorno J., Brigo F., Caggia E., Cagnetti C., Calvello C., Cesnik E., Chianale G., Ciampanelli D., Ciuffini R., Cocito D., Colella D., Contento M., Costa C., Cumbo E., D'Aniello A., Deleo F., DiFrancesco J.C., Di Giacomo R., Di Liberto A., Domina E., Dono F., Durante V., Elia M., Estraneo A., Evangelista G., Faedda M.T., Failli Y., Fallica E., Fattouch J., Ferrari A., Ferreri F., Fisco G., Fonti D., Fortunato F., Foschi N., Francavilla T., Galli R., Gazzina S., Giallonardo A.T., Giorgi F.S., Giuliano L., Habetswallner F., Izzi F., Kassabian B., Labate A., Luisi C., Magliani M., Maira G., Mari L., Marino D., Mascia A., Mazzeo A., Milano C., Meletti S., Nilo A., Orlando B., Paladin F., Pascarella M.G., Pastori C., Pauletto G., Peretti A., Perri G., Pezzella M., Piccioli M., Pignatta P., Pilolli N., Pisani F., Pisani L.R., Placidi F., Pollicino P., Porcella V., Pradella S., Puligheddu M., Quadri S., Quarato P.P., Quintas R., Renna R., Rizzo G.R., Rum A., Salamone E.M., Savastano E., Sessa M., Stokelj D., Tartara E., Tombini M., Tumminelli G., Vaudano A.E., Ventura M., Vigano I., Viglietta E., Vignoli A., Villani F., Zambrelli E., and Zummo L.

Subjects
Adult, Antiseizure medication, Brivaracetam, Cerebrovascular diseases, Focal seizures, Stroke, Settore MED/26, Antiseizure medication, Brivaracetam, Focal seizures, Stroke, Cerebrovascular diseases, Double-Blind Method, Drug Therapy, Seizures, Humans, Aged, Retrospective Studies, Epilepsy, General Medicine, Middle Aged, Pyrrolidinones, Treatment Outcome, Neurology, Italy, Combination, Anticonvulsants, Drug Therapy, Combination, Neurology (clinical)
Abstract

Objective: Post-stroke epilepsy (PSE) is one of the most common causes of acquired epilepsy and accounts for about 10-15% of all newly diagnosed epilepsy cases. However, evidence about the clinical profile of antiseizure medications in the PSE setting is currently limited. Brivaracetam (BRV) is a rationally developed compound characterized by high-affinity binding to synaptic vesicle protein 2A. The aim of this study was to assess the 12-month effectiveness and tolerability of adjunctive BRV in patients with PSE treated in a real-world setting. Methods: This was a subgroup analysis of patients with PSE included in the BRIVAracetam add-on First Italian netwoRk Study (BRIVAFIRST). The BRIVAFIRST was a 12-month retrospective, multicentre study including adult patients prescribed adjunctive BRV. Effectiveness outcomes included the rates of seizure response (≥50% reduction in baseline seizure frequency), seizure‐freedom, and treatment discontinuation. Safety and tolerability outcomes included the rate of treatment discontinuation due to adverse events (AEs) and the incidence of AEs. Results: Patients with PSE included in the BRIVAFIRST were 75 and had a median age of 57 (interquartile range, 42-66) years. The median daily doses of BRV at 3, 6, and 12 months from starting treatment were 100 (100-150) mg, 125 (100-200) mg and 100 (100-200) mg, respectively. At 12 months, 32 (42.7%) patients had a reduction in their baseline seizure frequency by at least 50%, and the seizure freedom rates was 26/75 (34.7%). During the 1-year study period, 10 (13.3%) patients discontinued BRV. The reasons of treatment withdrawal were insufficient efficacy in 6 (8.0%) patients and poor tolerability in 4 (5.3%) patients. Adverse events were reported by 13 (20.3%) patients and were rated as mild in 84.6% and moderate in 15.4% of cases. Significance: Adjunctive BRV was efficacious and generally well-tolerated when used in patients with PSE in clinical practice. Adjunctive BRV can be a suitable therapeutic option for patients with PSE.

Published
2022

2. Differences in visual information processing style between Idiopathic Generalized Epilepsy with and without photosensitivity

Author

Francesco Di Sabato, Carlo Di Bonaventura, Filippo Brighina, Marzia Buonfiglio, Giuliano Avanzini, Silvia Mandillo, Anna Teresa Giallonardo, Mariarita Albini, Buonfiglio M., Albini M., Mandillo S., Brighina F., Di Sabato F., Di Bonaventura C., Giallonardo A.T., and Avanzini G.

Subjects
medicine.medical_specialty, Audiology, Epilepsy, Reflex, Visual processing, Idiopathic generalized epilepsy, Behavioral Neuroscience, Epilepsy, Cognition, Photosensitive epilepsy, Photosensitivity, Idiopathic Generalized Epilepsy, Analytic cognitive style, Habituation, Auditory processing, medicine, Humans, Association (psychology), business.industry, Electroencephalography, medicine.disease, Neurology, Evoked Potentials, Visual, Epilepsy, Generalized, Neurology (clinical), Analysis of variance, business
Abstract

Purpose: Recently, altered visual cortical processes i.e., lack of habituation to visual evoked potentials (VEP), has been highlighted in both photosensitive epilepsy and in a specific i.e., analytic mode of processing visual inputs. In this study we aimed at evaluating the relationship between photosensitivity (PS) and analytic style of processing visual information, in a sample of 30 patients with Idiopathic Generalized Epilepsy (IGE) and matched healthy controls. Methods: At our Epilepsy unit of the Sapienza University of Rome, we consecutively enrolled 15 patients with IGE with PSand matched them with 15 patients with IGE without PS and 15 Healthy Volunteers. All patients underwent EEG recording in basal conditions during hyperventilation (3 Min), and intermittent light stimulation. The most effective frequencies comprised from 12 to 16 Hz. The instruments used to gather psychological cognitive behavioral data, consisted of participation in two tests: the Sternberg-Wagner Self-Assessment Inventory and the Mariani Learning Style Questionnaire. Results: Compared to controls, both IGE groups show significantly higher scores for the analytic style (One-way ANOVA, F(2,44) = 110.3, p < 0.0001). Epilepsy groups thereby showed very distinctive cognitive styles as measured with the Sternberg test. In the visual style, scores of the photosensitive Individuals with IGE were significantly higher than the non-photosensitive individuals with IGE (p < 0.0001, Tukey's post hoc test). Conclusions: An association between analytic style of processing visual information and PS in IGE has been shown. The common neurophysiological features between these two factors, suggest the possibility to evaluate this cognitive behavior as a potential target for nonpharmacological therapeutic strategies in photosensitive epilepsy.

Published
2021
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3. Genome-wide linkage meta-analysis identifies susceptibility loci at 2q34 and 13q31.3 for genetic generalized epilepsies

Author

EPICURE Consortium, Leu C., de Kovel C. G., Zara F., Striano P., Pezzella M., Robbiano A., Bianchi A., Coppola A., Giallonardo A. T., Beccaria F., Trenité D. K., Lindhout D., Gaus V., Schmitz B., Janz D., Weber Y. G., Becker F., Lerche H., Kleefuss Lie A. A., Hallman K., Kunz W. S., Elger C. E., Muhle H., Stephani U., Møller R. S., Hjalgrim H., Mullen S., Scheffer I. E., Berkovic S. F., Everett K. V., Gardiner M. R., Marini C., Guerrini R., Lehesjoki A. E., Siren A., Nabbout R., Baulac S., Leguern E., Serratosa J. M., Rosenow F., Feucht M., Unterberger I., Covanis A., Suls A., Weckhuysen S., Kaneva R., Caglayan H., Turkdogan D., Baykan B., Bebek N., Ozbek U., Hempelmann A., Schulz H., Rüschendorf F., Trucks H., Nürnberg P., Avanzini G., Koeleman B. P., Sander T., BISULLI, FRANCESCA, TINUPER, PAOLO, YÜCESAN, EMRAH, EPICURE Consortium, Leu C., de Kovel C.G., Zara F., Striano P., Pezzella M., Robbiano A., Bianchi A., Bisulli F., Coppola A., Giallonardo A.T., Beccaria F., Trenité D.K., Lindhout D., Gaus V., Schmitz B., Janz D., Weber Y.G., Becker F., Lerche H., Kleefuss-Lie A.A., Hallman K., Kunz W.S., Elger C.E., Muhle H., Stephani U., Møller R.S., Hjalgrim H., Mullen S., Scheffer I.E., Berkovic S.F., Everett K.V., Gardiner M.R., Marini C., Guerrini R., Lehesjoki A.E., Siren A., Nabbout R., Baulac S., Leguern E., Serratosa J.M., Rosenow F., Feucht M., Unterberger I., Covanis A., Suls A., Weckhuysen S., Kaneva R., Caglayan H., Turkdogan D., Baykan B., Bebek N., Ozbek U., Hempelmann A., Schulz H., Rüschendorf F., Trucks H., Nürnberg P., Avanzini G., Koeleman B.P., Sander T., and Tinuper P.

Subjects
Male, Chromosomes, Human, Pair 13, Genotype, Genetic Linkage, Chromosome Mapping, complex inheritance, Pedigree, genetic generalized epilepsy, myoclonic seizure, Phenotype, Genetic Loci, Chromosomes, Human, Pair 2, Humans, Epilepsy, Generalized, Family, Female, Genetic Predisposition to Disease, linkage analysis, absence seizure, Genome-Wide Association Study
Abstract

PURPOSE: Genetic generalized epilepsies (GGEs) have a lifetime prevalence of 0.3% with heritability estimates of 80%. A considerable proportion of families with siblings affected by GGEs presumably display an oligogenic inheritance. The present genome-wide linkage meta-analysis aimed to map: (1) susceptibility loci shared by a broad spectrum of GGEs, and (2) seizure type-related genetic factors preferentially predisposing to either typical absence or myoclonic seizures, respectively. METHODS: Meta-analysis of three genome-wide linkage datasets was carried out in 379 GGE-multiplex families of European ancestry including 982 relatives with GGEs. To dissect out seizure type-related susceptibility genes, two family subgroups were stratified comprising 235 families with predominantly genetic absence epilepsies (GAEs) and 118 families with an aggregation of juvenile myoclonic epilepsy (JME). To map shared and seizure type-related susceptibility loci, both nonparametric loci (NPL) and parametric linkage analyses were performed for a broad trait model (GGEs) in the entire set of GGE-multiplex families and a narrow trait model (typical absence or myoclonic seizures) in the subgroups of JME and GAE families. KEY FINDINGS: For the entire set of 379 GGE-multiplex families, linkage analysis revealed six loci achieving suggestive evidence for linkage at 1p36.22, 3p14.2, 5q34, 13q12.12, 13q31.3, and 19q13.42. The linkage finding at 5q34 was consistently supported by both NPL and parametric linkage results across all three family groups. A genome-wide significant nonparametric logarithm of odds score of 3.43 was obtained at 2q34 in 118 JME families. Significant parametric linkage to 13q31.3 was found in 235 GAE families assuming recessive inheritance (heterogeneity logarithm of odds = 5.02). SIGNIFICANCE: Our linkage results support an oligogenic predisposition of familial GGE syndromes. The genetic risk factor at 5q34 confers risk to a broad spectrum of familial GGE syndromes, whereas susceptibility loci at 2q34 and 13q31.3 preferentially predispose to myoclonic seizures or absence seizures, respectively. Phenotype- genotype strategies applying narrow trait definitions in phenotypic homogeneous subgroups of families improve the prospects of disentangling the genetic basis of common familial GGE syndromes.

Published
2012

4. Autosomal dominant lateral temporal epilepsy: absence of mutations in ADAM22 and Kv1 channel genes encoding LGI1-associated proteins

Author

Edoardo Ferlazzo, Salvatore Striano, Federica Pinardi, Amedeo Bianchi, Antonio Gambardella, Pasquale Striano, Simona Binelli, Giangennaro Coppola, Anna Teresa Giallonardo, Francesca Bisulli, Umberto Aguglia, Maurizio Elia, Carlo Nobile, Erica Diani, Valeria Vianello, Oriano Mecarelli, Gabriella Egeo, Barbara Castellotti, Paolo Tinuper, Carlo Di Bonaventura, Giorgia Bovo, Roberto Michelucci, Diani, E, Di Bonaventura, C, Mecarelli, O, Gambardella, A, Elia, M, Bovo, G, Bisulli, F, Pinardi, F, Binelli, S, Egeo, G, Castellotti, B, Striano, Pasquale, Striano, Salvatore, Bianchi, A, Ferlazzo, E, Vianello, V, Coppola, G, Aguglia, U, Tinuper, P, Giallonardo, At, Michelucci, R, Nobile, C., Diani E., Di Bonaventura C., Mecarelli O., Gambardella A., Elia M., Bovo G., Bisulli F., Pinardi F., Binelli S., Egeo G., Castellotti B., Striano P., Striano S., Bianchi A., Ferlazzo E., Vianello V., Coppola G., Aguglia U., Tinuper P., Giallonardo A.T., Michelucci R., and Nobile C.

Subjects
Male, Protein subunit, Population, DNA Mutational Analysis, Nerve Tissue Proteins, Biology, medicine.disease_cause, ADAM Proteins, genetics, DNA Mutational Analysis, methods, Epilepsy, Temporal Lobe, genetics, Family Health, Female, Genetic Testing, methods, Humans, Male, Middle Aged, Nerve Tissue Proteins, genetics, Polymorphism, Restriction Fragment Length, Proteins, genetics, Shaker Superfamily of Potassium Channels, genetics, methods, Exon, adam22 receptor, association studies, autosomal dominant lateral temporal epilepsy, kv1 channel, lgi1, Genetic, Neurotransmitter receptor, medicine, Humans, Genetic Testing, Polymorphism, Kv1 channel, education, Gene, Autosomal dominant lateral temporal epilepsy, Association studies, Genetics, Family Health, Mutation, education.field_of_study, Epilepsy, Genetic heterogeneity, ADAM22, ADAM22 receptor, Intracellular Signaling Peptides and Proteins, Proteins, Middle Aged, Restriction Fragment Length, Neurology, Epilepsy, Temporal Lobe, Shaker Superfamily of Potassium Channels, LGI1, Female, Neurology (clinical), Polymorphism, Restriction Fragment Length
Abstract

Mutations in the LGI1 gene are linked to autosomal dominant lateral temporal epilepsy (ADTLE) in about half of the families tested, suggesting that ADLTE is genetically heterogeneous. Recently, the Lgi1 protein has been found associated with different protein complexes and two distinct molecular mechanisms possibly underlying ADLTE have been hypothesized: the one recognizes Lgi1 as a novel subunit of the presynaptic Kv1 potassium channel implicated in the regulation of channel inactivation, the other suggests that Lgi1 acts as a ligand that selectively binds to the postsynaptic receptor ADAM22, thereby regulating the glutamate-AMPA neurotransmission. Both mechanisms imply that LGI1 mutations result in alteration of synaptic currents, though of different types. Since their protein products have been found associated with Lgi1, the Kv1 channel subunit genes KCNA1, KCNA4, and KCNAB1 and ADAM22 can be considered strong candidates for ADLTE. We sequenced their coding exons and flanking splice sites in the probands of 9 carefully ascertained ADLTE families negative for LGI1 mutations. We failed to detect any mutation segregating with the disease, but identified several previously unreported polymorphisms. An association study of four non-synonymous variants (three found in ADAM22, one in KCNA4) in a population of 104 non-familial lateral temporal epilepsy cases did not show any modification of susceptibility to this disorder. Altogether, our results suggest that neither ADAM22 nor any of the three Kv1 channel genes are major causative genes for ADLTE.

Published
2007

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