Journal articles: 'Generalized Epilepsy'

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Sullivan, Joseph E., and Dennis J. Dlugos. "Idiopathic generalized epilepsy." Current Treatment Options in Neurology 6, no. 3 (June 2004): 231–42. http://dx.doi.org/10.1007/s11940-004-0015-6.

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Agashe, Shruti, Gregory Worrell, Jeffrey Britton, Katherine Noe, Anthony Ritaccio, Elaine C. Wirrell, Katherine C. Nickels, Gregory D. Cascino, and David Burkholder. "Cenobamate in Generalized Epilepsy and Combined Generalized and Focal Epilepsy." Neurology: Clinical Practice 13, no. 2 (February 15, 2023): e200133. http://dx.doi.org/10.1212/cpj.0000000000200133.

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Background and ObjectivesCenobamate (CNB) is a United States Food and Drug Administration–approved antiseizure medication (ASM) for focal-onset seizures; however, its potential clinical effectiveness as a broad-spectrum ASM is not established. CNB has a proposed dual mechanism of action with preferential blockade of persistent sodium currents and positive allosteric modulation of the γ-aminobutyric acid-A (GABA-A) receptor. We evaluated the efficacy of CNB in drug refractory patients with genetic generalized epilepsies (GGE) or combined generalized and focal epilepsies (CGFE), including developmental and epileptic encephalopathies.MethodsWe performed a retrospective review and identified the following: cohort 1 (n = 4) with GGE, of which 2 patients had idiopathic generalized epilepsy, and cohort 2 with CGFE (n = 9), of which 4 patients had Lennox-Gastaut syndrome and 1 had Dravet syndrome.ResultsIn cohort 1, all 3 patients with frequent generalized tonic-clonic seizures (GTCs) had a greater than 50% reduction in GTCs. In cohort 2, reduction in both generalized and focal-onset seizures was noted. In these groups together, the mean reduction of all seizure types was 58%, and ≥50% responder rate was 70% (SD = ±34.16, median = 50%). No worsening of generalized-onset seizures occurred in either cohort. Seventy-seven percent of patients experienced side effects, warranting a modification of treatment managed by slower titration, dose reduction of CNB, or discontinuing other ASMs.DiscussionIn our retrospective case series, CNB seems to be an effective ASM for patients with drug-resistant GGE and CGFE. The ongoing CNB trial assessing effectiveness for primary GTCs will provide more data on generalized-onset seizures.Classification of EvidenceThis study provides Class IV evidence that CNB in generalized epilepsy and combined generalized and focal epilepsy reduces seizure frequency.

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Jayaram, Shoba, Modhi Alkhaldi, and Asim Shahid. "The Role and Controversies of Electroencephalogram in Focal versus Generalized Epilepsy." Journal of Pediatric Epilepsy 10, no. 02 (February 19, 2021): 058–64. http://dx.doi.org/10.1055/s-0041-1722869.

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AbstractAs early in 1935, Gibbs et al described electroencephalogram (EEG) features of large slow waves seen in “petit mal” seizures and change in background rhythm to a higher frequency, greater amplitude pattern in “grand mal” seizures. Studies have shown many typical EEG features in focal onset as well as generalized epilepsies.2 3 It is usually easy to delineate focal epilepsy cases when EEG onset of seizures is clear as seen in Benign focal epileptiform discharges of childhood.4 However, it is not uncommon to see cases where epileptiform discharges are not very clear. For example, there can be secondary bilateral synchrony or generalized onset of epileptiform discharges in some cases of focal epilepsy5 and nongeneralized EEG features is cases of generalized epilepsy like absence seizures.6 The awareness of occurrence of focal clinical and EEG features in generalized epilepsy is particularly important to help to select appropriate AEDs and also to avoid inappropriate consideration for epilepsy surgery.7 Lüders et al8 have shown that multiple factors like electroclinical seizure evolution, neuroimaging (both functional and anatomical) have to be analyzed in depth before defining an epileptic syndrome. Here, we are providing few examples of different situations where it is still mysterious to figure out focal onset seizures with secondary generalization versus primary generalized epilepsy.

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Ibrahim Abdullah Mahmood, Ahmed Tahseen Muslim, and Hussein Ghani Kaddoori. "The utility of hematological indices in differentiation between general and focal onset epilepsy." Biomedicine 42, no. 1 (March 5, 2022): 64–71. http://dx.doi.org/10.51248/.v42i1.890.

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Introduction and Aim: Epilepsy is one of the most common neurological disorders with mainly focal and generalized onset types. Discrimination between these types is of paramount importance because the prescription of antiepileptic drugs (AEDs) depends on such decimation. Currently this made mainly upon the medical history of the patient. The aim of the study is to evaluate the role of hematological indices in discrimination between focal and generalize onset epilepsy. Patients and Methods: This cross-sectional study included a total of 100 patients with epilepsy (mean age 21.44±10.5, range 6-52, 67 males and 33 females). Blood samples were collected for the participant and complete blood count (CBC) was performed. Furthermore, serum concentration of K+ and Na+ was determined. Results: There were 38 patients with generalized and 62 patients with focal onset epilepsy. In multivariate initial analysis, each of mean platelet volume (MPV) (odds ratio (OR)= 2.56, 95%CI=1.09-13.22, p= 0.046) and serum Na+ (OR= 3.85, 95%CI=1.13-13.19, p= 0.032) were significantly associated with generalized onset epilepsy. Furthermore, two AEDs: carbamazepine and valproic acid were also independently associated with generalized and local onset epilepsy, respectively. Conclusion: These data indicate the possible utility of MPV in the discrimination between generalized and focal onset epilepsy. However, further studies are required for more reliable conclusions.

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Koepp, M. J. "Juvenile myoclonic epilepsy - a generalized epilepsy syndrome?" Acta Neurologica Scandinavica 112, s181 (December 2005): 57–62. http://dx.doi.org/10.1111/j.1600-0404.2005.00511.x.

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Millichap, J. Gordon. "Idiopathic Generalized Epilepsy Syndromes." Pediatric Neurology Briefs 9, no. 9 (September 1, 1995): 68. http://dx.doi.org/10.15844/pedneurbriefs-9-9-7.

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Pedersen, Mangor, Magdalena Kowalczyk, Amir Omidvarnia, Piero Perucca, Samuel Gooley, Steven Petrou, Ingrid E. Scheffer, Samuel F. Berkovic, and Graeme D. Jackson. "Human GABRG2 generalized epilepsy." Neurology Genetics 5, no. 4 (June 7, 2019): e340. http://dx.doi.org/10.1212/nxg.0000000000000340.

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ObjectiveTo map functional MRI (fMRI) connectivity within and between the somatosensory cortex, putamen, and ventral thalamus in individuals from a family with a GABAergic deficit segregating with febrile seizures and genetic generalized epilepsy.MethodsWe studied 5 adults from a family with early-onset absence epilepsy and/or febrile seizures and a GABAA receptor subunit gamma2 pathogenic variant (GABRG2[R43Q]) vs 5 age-matched controls. We infer differences between participants with the GABRG2 pathogenic variant and controls in resting-state fMRI connectivity within and between the somatosensory cortex, putamen, and ventral thalamus.ResultsWe observed increased fMRI connectivity within the somatosensory cortex and between the putamen and ventral thalamus in all individuals with the GABRG2 pathogenic variant compared with controls. Post hoc analysis showed less pronounced changes in fMRI connectivity within and between the primary visual cortex and precuneus.ConclusionsAlthough our sample size was small, this preliminary study suggests that individuals with a GABRG2 pathogenic variant, raising risk of febrile seizures and generalized epilepsy, display underlying increased functional connectivity both within the somatosensory cortex and in striatothalamic networks. This human network model aligns with rodent research and should be further validated in larger cohorts, including other individuals with generalized epilepsy with and without known GABA pathogenic variants.

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Fujikawa, D. G. "Generalized Epilepsy: Neurobiological Approaches." Neurology 42, no. 6 (June 1, 1992): 1261. http://dx.doi.org/10.1212/wnl.42.6.1261-b.

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Dugan, P., C. Carlson, J. Bluvstein, D. J. Chong, D. Friedman, and H. E. Kirsch. "Auras in generalized epilepsy." Neurology 83, no. 16 (September 17, 2014): 1444–49. http://dx.doi.org/10.1212/wnl.0000000000000877.

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Avoli, M. "Feline generalized penicillin epilepsy." Italian Journal of Neurological Sciences 16, no. 1-2 (March 1995): 79–82. http://dx.doi.org/10.1007/bf02229078.

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Zempel, J. M., and T. Mano. "Myoclonic atonic epilepsy: Another generalized epilepsy syndrome that is "not so" generalized." Neurology 82, no. 17 (April 2, 2014): 1486–87. http://dx.doi.org/10.1212/wnl.0000000000000368.

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Triantafyllou, Nikolaos I., Stergios Gatzonis, Evangelia Kararizou, and Charalampos C. Papageorgiou. "Patterns of depressive symptoms in epilepsy." Arquivos de Neuro-Psiquiatria 71, no. 4 (April 2013): 213–15. http://dx.doi.org/10.1590/0004-282x20130004.

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Objective: The purpose of this study was to determine the nature and extent of depressive symptoms among patients with epilepsy. Methods: Ninety patients were investigated over a three-month period: 42 were suffering from generalized epilepsy, 29 from focal epilepsy and 19 from undetermined epilepsy. All completed the Zung self-rating scale for assessment of the depressive symptoms. Results: Sixty-seven patients felt stigmatized because of epilepsy (67%): 73.6% in the undetermined epilepsy group, 55.1% in the focal epilepsy group and 88% in the generalized epilepsy group. Moreover, among the 90 epileptic patients studied, symptoms of irritability, indecisiveness, personal devaluation and emptiness showed a constant increasing trend for their presence from the undetermined epilepsy group through the generalized epilepsy group to the focal epilepsy group. Conclusions: These findings indicate that although the focal epilepsy patients felt less stigmatized, they did not differ greatly in terms of depressive symptoms, in relation to the undetermined epilepsy and generalized epilepsy patients.

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Cornejo-Sanchez, Diana M., Jaime Carrizosa-Moog, Dagoberto Cabrera-Hemer, Rodrigo Solarte-Mila, Christhian Gomez-Castillo, Rhys Thomas, Suzanne M. Leal, William Cornejo-Ochoa, and Nicolas Pineda-Trujillo. "Sleepwalking and Sleep Paralysis: Prevalence in Colombian Families With Genetic Generalized Epilepsy." Journal of Child Neurology 34, no. 9 (April 23, 2019): 491–98. http://dx.doi.org/10.1177/0883073819842422.

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Background: Sleep deprivation commonly increases seizure frequency in patients with genetic generalized epilepsy, though it is unknown whether there is an increased prevalence of sleepwalking or sleep paralysis in genetic generalized epilepsy patients. Establishing this could provide insights into the bio-mechanisms or genetic architecture of both disorders. The aim of this study was to determine the prevalence of sleepwalking and sleep paralysis in a cohort of patients with genetic generalized epilepsy and their relatives in extended families. Methods: A structured interview based on International League Against Epilepsy (ILAE) and International Classification of Sleep Disorders (ICSD-3) criteria was applied to 67 index cases and their relatives to determine genetic generalized epilepsy subtypes and assess the occurrence of sleepwalking or sleep paralysis. Bivariate analysis was performed using chi-square and Fisher exact tests. Results: The prevalence of sleepwalking and sleep paralysis was 15.3% (95% confidence interval 12.1-18.9) and 11.7% (95% confidence interval 8.7-15.3), respectively. Unusually, no sleepwalkers were found among individuals displaying epilepsy with generalized tonic-clonic seizures. Approximately a quarter of the patients had either parasomnia or genetic generalized epilepsy. Over half the genetic generalized epilepsy families had at least 1 individual with sleepwalking, and more than 40% of the families had one individual with sleep paralysis. Conclusion: The prevalence of sleepwalking or sleep paralysis is reported for individuals with genetic generalized epilepsy and their relatives. The co-existence of either parasomnia in the genetic generalized epilepsy patients and the co-aggregation within their families let suggest that shared heritability and pathophysiological mechanisms exist between these disorders. We hypothesize that sleepwalking/sleep paralysis and genetic generalized epilepsy could be variable expression of genes in shared pathways.

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Assadsangabi, Reza, Arzu Ozturk, Trishna Kantamneni, Nazarin Azizi, Shailesh M. Asaikar, and Lotfi Hacein-Bey. "Neuroimaging of Childhood Epilepsy: Focal versus Generalized Epilepsy." Journal of Pediatric Epilepsy 10, no. 02 (February 2, 2021): 065–80. http://dx.doi.org/10.1055/s-0040-1722301.

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AbstractNeuroimaging plays an increasingly crucial role in delineating the pathophysiology, and guiding the evaluation, management and monitoring of epilepsy. Imaging contributes to adequately categorizing seizure/epilepsy types in complex clinical situations by demonstrating anatomical and functional changes associated with seizure activity. This article reviews the current status of multimodality neuroimaging in the pediatric population, including focal lesions which may result in focal epileptic findings, focal structural abnormalities that may manifest as generalized epileptiform discharges, and generalized epilepsy without evidence of detectable focal abnormalities.

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Niestroj, Lisa-Marie, Eduardo Perez-Palma, Daniel P. Howrigan, Yadi Zhou, Feixiong Cheng, Elmo Saarentaus, Peter Nürnberg, et al. "Epilepsy subtype-specific copy number burden observed in a genome-wide study of 17 458 subjects." Brain 143, no. 7 (June 22, 2020): 2106–18. http://dx.doi.org/10.1093/brain/awaa171.

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Abstract Cytogenic testing is routinely applied in most neurological centres for severe paediatric epilepsies. However, which characteristics of copy number variants (CNVs) confer most epilepsy risk and which epilepsy subtypes carry the most CNV burden, have not been explored on a genome-wide scale. Here, we present the largest CNV investigation in epilepsy to date with 10 712 European epilepsy cases and 6746 ancestry-matched controls. Patients with genetic generalized epilepsy, lesional focal epilepsy, non-acquired focal epilepsy, and developmental and epileptic encephalopathy were included. All samples were processed with the same technology and analysis pipeline. All investigated epilepsy types, including lesional focal epilepsy patients, showed an increase in CNV burden in at least one tested category compared to controls. However, we observed striking differences in CNV burden across epilepsy types and investigated CNV categories. Genetic generalized epilepsy patients have the highest CNV burden in all categories tested, followed by developmental and epileptic encephalopathy patients. Both epilepsy types also show association for deletions covering genes intolerant for truncating variants. Genome-wide CNV breakpoint association showed not only significant loci for genetic generalized and developmental and epileptic encephalopathy patients but also for lesional focal epilepsy patients. With a 34-fold risk for developing genetic generalized epilepsy, we show for the first time that the established epilepsy-associated 15q13.3 deletion represents the strongest risk CNV for genetic generalized epilepsy across the whole genome. Using the human interactome, we examined the largest connected component of the genes overlapped by CNVs in the four epilepsy types. We observed that genetic generalized epilepsy and non-acquired focal epilepsy formed disease modules. In summary, we show that in all common epilepsy types, 1.5–3% of patients carry epilepsy-associated CNVs. The characteristics of risk CNVs vary tremendously across and within epilepsy types. Thus, we advocate genome-wide genomic testing to identify all disease-associated types of CNVs.

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Knowles, Juliet K., Haojun Xu, Caroline Soane, Ankita Batra, Tristan Saucedo, Eleanor Frost, Lydia T. Tam, et al. "Maladaptive myelination promotes generalized epilepsy progression." Nature Neuroscience 25, no. 5 (May 2022): 596–606. http://dx.doi.org/10.1038/s41593-022-01052-2.

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AbstractActivity-dependent myelination can fine-tune neural network dynamics. Conversely, aberrant neuronal activity, as occurs in disorders of recurrent seizures (epilepsy), could promote maladaptive myelination, contributing to pathogenesis. In this study, we tested the hypothesis that activity-dependent myelination resulting from absence seizures, which manifest as frequent behavioral arrests with generalized electroencephalography (EEG) spike-wave discharges, promote thalamocortical network hypersynchrony and contribute to epilepsy progression. We found increased oligodendrogenesis and myelination specifically within the seizure network in two models of generalized epilepsy with absence seizures (Wag/Rij rats and Scn8a+/mut mice), evident only after epilepsy onset. Aberrant myelination was prevented by pharmacological seizure inhibition in Wag/Rij rats. Blocking activity-dependent myelination decreased seizure burden over time and reduced ictal synchrony as assessed by EEG coherence. These findings indicate that activity-dependent myelination driven by absence seizures contributes to epilepsy progression; maladaptive myelination may be pathogenic in some forms of epilepsy and other neurological diseases.

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Leu, Costin, Remi Stevelink, Alexander W. Smith, Slavina B. Goleva, Masahiro Kanai, Lisa Ferguson, Ciaran Campbell, et al. "Polygenic burden in focal and generalized epilepsies." Brain 142, no. 11 (October 14, 2019): 3473–81. http://dx.doi.org/10.1093/brain/awz292.

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Abstract Rare genetic variants can cause epilepsy, and genetic testing has been widely adopted for severe, paediatric-onset epilepsies. The phenotypic consequences of common genetic risk burden for epilepsies and their potential future clinical applications have not yet been determined. Using polygenic risk scores (PRS) from a European-ancestry genome-wide association study in generalized and focal epilepsy, we quantified common genetic burden in patients with generalized epilepsy (GE-PRS) or focal epilepsy (FE-PRS) from two independent non-Finnish European cohorts (Epi25 Consortium, n = 5705; Cleveland Clinic Epilepsy Center, n = 620; both compared to 20 435 controls). One Finnish-ancestry population isolate (Finnish-ancestry Epi25, n = 449; compared to 1559 controls), two European-ancestry biobanks (UK Biobank, n = 383 656; Vanderbilt biorepository, n = 49 494), and one Japanese-ancestry biobank (BioBank Japan, n = 168 680) were used for additional replications. Across 8386 patients with epilepsy and 622 212 population controls, we found and replicated significantly higher GE-PRS in patients with generalized epilepsy of European-ancestry compared to patients with focal epilepsy (Epi25: P = 1.64×10−15; Cleveland: P = 2.85×10−4; Finnish-ancestry Epi25: P = 1.80×10−4) or population controls (Epi25: P = 2.35×10−70; Cleveland: P = 1.43×10−7; Finnish-ancestry Epi25: P = 3.11×10−4; UK Biobank and Vanderbilt biorepository meta-analysis: P = 7.99×10−4). FE-PRS were significantly higher in patients with focal epilepsy compared to controls in the non-Finnish, non-biobank cohorts (Epi25: P = 5.74×10−19; Cleveland: P = 1.69×10−6). European ancestry-derived PRS did not predict generalized epilepsy or focal epilepsy in Japanese-ancestry individuals. Finally, we observed a significant 4.6-fold and a 4.5-fold enrichment of patients with generalized epilepsy compared to controls in the top 0.5% highest GE-PRS of the two non-Finnish European cohorts (Epi25: P = 2.60×10−15; Cleveland: P = 1.39×10−2). We conclude that common variant risk associated with epilepsy is significantly enriched in multiple cohorts of patients with epilepsy compared to controls—in particular for generalized epilepsy. As sample sizes and PRS accuracy continue to increase with further common variant discovery, PRS could complement established clinical biomarkers and augment genetic testing for patient classification, comorbidity research, and potentially targeted treatment.

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Barreto, José Roberto Santiago, Regina Maria França Fernandes, and Américo Ceiki Sakamoto. "Correlation of sleep macrostructure parameters and idiopathic epilepsies." Arquivos de Neuro-Psiquiatria 60, no. 2B (June 2002): 353–57. http://dx.doi.org/10.1590/s0004-282x2002000300002.

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Sleep and epilepsy share some common mechanisms. The objective of the present investigation was to study the macrostructure of sleep in patients with idiopathic epilepsies, focal and generalized, comparing these two groups to each other and to a control group of 12 individuals without epilepsy. A total of 35 polysomnographies were performed, 12 of them in the control group, 10 in patients with idiopathic generalized epilepsies, and 13 in patients with idiopathic focal epilepsies. Antiepileptic medications were maintained for ethical reasons. The group with idiopathic focal epilepsy showed an increase in the total recording time (p = 0.04) and the group with idiopathic generalized epilepsy had a reduction of phase 4 NREM sleep. The efficiency of total sleep period and of total sleep time was also lower in the group with idiopathic generalized epilepsy (p = 0.03 in both cases). We concluded that the group with idiopathic generalized epilepsy presents sleep of poorer quality, whereas the group with idiopathic focal epilepsy presents a tendency toward an excessive somnolence.

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Jannat Ara, Kazi, Abu Nasir Rizvi, Kanuj Kumar Barman, and Khair M. Sobhan. "A prospective observational study on understanding of idiopathic generalized epilepsies namely juvenile myoclonic epilepsy and epilepsy with generalized tonic-clonic seizure alone by electroencephalogram with updated terminology in a tertiary care hospital." International Journal of Research in Medical Sciences 11, no. 1 (December 30, 2022): 47. http://dx.doi.org/10.18203/2320-6012.ijrms20223622.

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Background: In 2017, the international league against epilepsy (ILAE) classification of epilepsies described the “genetic generalized epilepsies”, which contained the “idiopathic generalized epilepsies”. This study delineates the four syndromes comprising the IGEs: childhood absence epilepsy, juvenile absence epilepsy, juvenile myoclonic epilepsy (JME), and epilepsy with generalized tonic-clonic seizures alone (GTCA). JME patients usually present with myoclonic seizures, and GTCA patients present with GTCS only after awakening from sleep. Aim of the study was to identify the differences between juvenile myoclonic epilepsy and epilepsy with generalized tonic-clonic seizures alone by semiology and EEG with updated terminology under the observation of the clinicians.Methods: This was a prospective observational study and was conducted in the epilepsy clinic, department of neurology, Bangabandhu Sheikh Mujib medical university, from February 2021 to July 2022. The sample size was 60. Results: Among 60 patients, family history was present in 12 (20%) and 6 (10%) JME and GTCA patients, respectively. In this study, the EEG finding of generalized spike-wave (2.5-5.5 Hz) was seen in 26 (43%) and 19 (32%) among JME and GTCA patients, respectively. Generalized Polyspike wave (2.5-5.5 Hz) was seen in 26 (43%) JME patients, and EEG was normal in 15 out of 60 patients of epilepsy. In EEG findings, 2.5-5.5 Hz generalized spike-wave should be diagnosed in JME and GTCA patients as a special group of IGEs. Conclusions: In this study, we have recognized and differentiated between juvenile myoclonic epilepsy and generalized tonic-clonic seizures alone by semiology and EEG in IGE syndromes as a special grouping among the IGEs is helpful as they carry prognostic and therapeutic implications.

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Millichap, J. Gordon. "Idiopathic Generalized Epilepsy with Hemiconvulsions." Pediatric Neurology Briefs 15, no. 2 (February 1, 2001): 14. http://dx.doi.org/10.15844/pedneurbriefs-15-2-8.

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Millichap, J. Gordon. "Hypothalamic Hamartoma and Generalized Epilepsy." Pediatric Neurology Briefs 17, no. 3 (March 1, 2003): 19. http://dx.doi.org/10.15844/pedneurbriefs-17-3-2.

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Kawai, Itsuo, Kazuichi Yagi, Yushi Inoue, and Yoichi Numata. "Primary Generalized Epilepsy in Adolescence." Psychiatry and Clinical Neurosciences 40, no. 3 (September 1986): 323–27. http://dx.doi.org/10.1111/j.1440-1819.1986.tb03154.x.

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Willis, Erin, and Debopam Samanta. "Generalized Epilepsy Syndromes of Adolescence." Journal of Pediatric Epilepsy 04, no. 03 (August 17, 2015): 096–101. http://dx.doi.org/10.1055/s-0035-1556738.

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Drury, Ivo, and Thomas R. Henry. "Ictal Patterns in Generalized Epilepsy." Journal of Clinical Neurophysiology 10, no. 3 (July 1993): 268–80. http://dx.doi.org/10.1097/00004691-199307000-00003.

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Rossetti, Andrea O. "Dostoevsky’s epilepsy: Generalized or focal?" Epilepsy & Behavior 8, no. 2 (March 2006): 446–47. http://dx.doi.org/10.1016/j.yebeh.2005.11.009.

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Willoughby, John O., Lorraine Mackenzie, Andrei Medvedev, and Jennifer J. Hiscock. "Generalized convulsive epilepsy: possible mechanisms." Journal of Clinical Neuroscience 6, no. 3 (May 1999): 189–94. http://dx.doi.org/10.1016/s0967-5868(99)90500-3.

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Futatsugi, Yoshio, and James J. Riviello Jr. "Mechanisms of generalized absence epilepsy." Brain and Development 20, no. 2 (March 1998): 75–79. http://dx.doi.org/10.1016/s0387-7604(97)00107-1.

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SULLIVAN, MICHELE G. "Symptomatic Generalized Epilepsy Deters Development." Clinical Psychiatry News 33, no. 4 (April 2005): 38. http://dx.doi.org/10.1016/s0270-6644(05)70148-x.

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Hosford, David A. "Models of primary generalized epilepsy." Current Opinion in Neurology 8, no. 2 (April 1995): 121–25. http://dx.doi.org/10.1097/00019052-199504000-00006.

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Ammar Mohammed Hallumy, Khalid Saoud Saleh, and Mays Altai. "Incidence and Associated Factors of Juvenile Myoclonic Epilepsy among Idiopathic Generalized Epilepsy." Tikrit Journal of Pharmaceutical Sciences 16, no. 1 (December 16, 2022): 1–8. http://dx.doi.org/10.25130/tjphs.2022.16.1.1.1.8.

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Juvenile myoclonic epilepsy (JME) is widely recognized presumed genetic, electroclinical idiopathic generalized epilepsy (IGE) syndrome. The prevalence of JME is about 18% of IGEs. However, there is a considerable variation in different settings.Aims: to determine the incidence and associated factors of JME among patients with IGEs.Patients and Methods: This retrospective study included a total of 52 patients with electro-clinical feature of IGE. All enrolled patients were undergone a three-hour video electroencephalography (EEG). JME was diagnosed on the basis of JME consensus definition clinical criteria class II. The demographic and clinical characteristics of the patients were abstracted from their records.Results: The most common epilepsy syndrome of IGE was generalized tonic-clonic seizure (GTCS) only affecting (32.7%) followed by juvenile absence epilepsy (JAE) (25%), JME and JME only (each 17.3%) and Generalized myoclonic epilepsy and generalized tonic-clonic (GMEGTC) (13.46%). All JME patients were females (100%) compared with 69.77% of the patients in other IGE syndromes with a highly significant difference. According to EEG results, 8 patients (88.89%) of JME patients had generalized polyspikes, and two patient (22.22%) showed generalized spikes and waves (3/second spike and wave complex). One patient (11.11%) two EEG findings (polyspike and generalized spike and waves)Conclusions: JME can affect adolescents and young adults and it can effect child age group. It is distinguished by the occurrence of myoclonic seizures, characteristic spike-and-wave EEG pattern at 4-6 Hz, and more common in females than males.

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Fountain, Nathan B. "A Frontal Assault on the Generalized Nature of Juvenile Myoclonic Epilepsy." Epilepsy Currents 8, no. 6 (October 6, 2008): 152–53. http://dx.doi.org/10.1111/j.1535-7511.2008.00276.x.

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Frontal Cognitive Dysfunction in Juvenile Myoclonic Epilepsy. Piazzini A, Turner K, Vignoli A, Canger R, Canevini M P. Epilepsia 2008;49(4):657–662. PURPOSE: The aim of the present study was to investigate the possible frontal cognitive dysfunction in patients with juvenile myoclonic epilepsy (JME) and to compare the results with those of patients with frontal lobe epilepsy (FLE) and temporal lobe epilepsy (TLE), as well as with controls. METHODS: A total of 50 patients with JME, 40 patients with FLE, 40 patients with TLE, and 40 normal controls, all matched for age, education, and IQ, were administered tests to assess frontal functions (the Word Fluency Test and the Wisconsin Card Sorting Test [WCST]). All participants had a normal intelligence level based on the Wechsler Adult Intelligence Scale, and did not take medications other than antiepileptics (AEDs) or have a psychiatric history. RESULTS: Patients with JME had severe impairment in all administered tasks, similar to that of patients with FLE; TLE patients and controls followed in order. Multiple regression analysis did not disclose any significant effect of clinical variables on the cognitive deficits. DISCUSSION: These results clearly suggest that JME patients can show some frontal dysfunction, which may affect both epileptogenic features and cognitive processes. Further studies are needed to confirm these findings.

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Ba-Armah, Duaa, Puneet Jain, Robyn Whitney, Elizabeth Donner, James Drake, Cristina Go, Rajesh Ramachandran Nair, et al. "Misleading Focal Clinical, Neurophysiologic, and Imaging Features in 2 Children With Generalized Epilepsy Who Underwent Invasive Electroencephalographic (EEG) Monitoring." Journal of Child Neurology 35, no. 6 (February 16, 2020): 418–24. http://dx.doi.org/10.1177/0883073819901228.

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Children and adults with genetic generalized epilepsy may have focal clinical seizure symptoms as well as electroencephalographic (EEG) findings. This may pose a diagnostic challenge to clinicians, especially when concomitant focal neuroimaging findings exist and the epilepsy is medically refractory. We sought to highlight the challenges that clinicians may face through the description of 2 children with suspected genetic generalized epilepsy who had both focal seizure symptoms and EEG/neuroimaging findings and underwent invasive EEG monitoring. Ultimately, invasive monitoring failed to demonstrate a focal origin for the seizures in both cases, and instead confirmed the presence of genetic generalized epilepsy. We demonstrate that ≥3-Hz generalized monomorphic spike and waves are less likely to represent secondary bilateral synchrony, that focal neuroimaging findings may not always be causal and that repeated hyperventilation is an essential activation procedure for genetic generalized epilepsy.

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Nicolson, Andrew, David W. Chadwick, and David F. Smith. "The Coexistence of Idiopathic Generalized Epilepsy and Partial Epilepsy." Epilepsia 45, no. 6 (June 2004): 682–85. http://dx.doi.org/10.1111/j.0013-9580.2004.45003.x.

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Dreifuss, Fritz E. "Juvenile Myoclonic Epilepsy: Characteristics of a Primary Generalized Epilepsy." Epilepsia 30, s4 (December 1989): S1—S7. http://dx.doi.org/10.1111/j.1528-1157.1989.tb05832.x.

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Kendis, Hallie, Kelly Baron, Stephan U. Schuele, Bhavita Patel, and Hrayr Attarian. "Chronotypes in Patients with Epilepsy: Does the Type of Epilepsy Make a Difference?" Behavioural Neurology 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/941354.

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Circadian rhythms govern all biological functions. Circadian misalignment has a major impact on health. Late chronotype is a risk factor for circadian misalignment which in turn can affect the control of seizures in epilepsy patients. We compared a group of 87 confirmed epilepsy patients regardless of subtypes with age- and sex-matched healthy controls. We compared generalized epilepsy patients with localization related epilepsy patients and with healthy controls. We found that primary generalized epilepsy patients were 5 times more likely to have a late chronotype than healthy controls. We did not find any significant differences between localization related epilepsy patients and healthy controls or between the overall epilepsy cohort and healthy controls. Generalized epilepsy patients are more likely to be evening types as compared to those with focal epilepsy or subjects without epilepsy. Epilepsy patients do not experience the same age related increase in morningness as do age-matched healthy controls. This is important in regard to timing of AED, identifying and preventing sleep deprivation, and integrating chronotype evaluations and chronotherapy in comprehensive epilepsy care. Further studies, using objective phase markers or the impact of chronotherapy on seizure control, are necessary.

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Sapkota, Sanjeeb, Rosemarie Kobau, Daniel M. Pastula, and Matthew M. Zack. "People with epilepsy are diagnosed most often with unspecified epilepsy, followed by focal epilepsy, generalized convulsive epilepsy, and generalized nonconvulsive epilepsy—US MarketScan data, 2010–2015." Epilepsy & Behavior 79 (February 2018): 244–46. http://dx.doi.org/10.1016/j.yebeh.2017.11.004.

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Duaa, BM, A. Ye, S. Doesburg, H. Otsubo, and A. Ochi. "A multi-modality approach to identifying primary generalized epilepsy that can mimic focal epilepsy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 42, S1 (May 2015): S22. http://dx.doi.org/10.1017/cjn.2015.114.

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Introduction: Evaluating the suitability for surgery in patients with epilepsy requires determining if the epilepsy is focal or generalized. Presurgical workups can indicate focal epilepsy in certain cases of generalized epilepsy (GE). The purpose of this study was to identify distinctive features which characterize patients with primary GE that mimics focal epilepsy. Method: We retrospectively identified 19 children with generalized interictal discharges during scalp video-EEG (SVEEG) and underwent invasive monitoring and/or epilepsy surgery. Two children did not undergo resective surgery due to final diagnosis of primary GE (Group A). Seventeen children underwent a resective surgery (Group B). Scalp video-EEG, MEG, MRI, and intracranial video EEG (IVEEG) were reviewed. Results: On (SVEEG), the frequency of generalized spike-and-waves (GSW) was 3Hz in Group A and 1.5-2.5Hz in Group B. Group A had only absence seizures , whereas 80% in Group B had multiple types of seizures. Both groups had lateralized MEG dipoles. One patient in Group A had a focal MRI abnormality. In Group A, IVEEG showed GSW of 3 Hz frequency with inconsistent leading. In Group B, IVEEG showed consistent localization of ictal and interictal high frequency oscillations. Conclusion: Children with generalized 3 Hz spike-and-waves and only absence seizures may be a contraindication of resective surgery even though some presurgical workup shows focality.

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Najafi, Tahereh, Rosmina Jaafar, Rabani Remli, and Wan Asyraf Wan Zaidi. "A Classification Model of EEG Signals Based on RNN-LSTM for Diagnosing Focal and Generalized Epilepsy." Sensors 22, no. 19 (September 25, 2022): 7269. http://dx.doi.org/10.3390/s22197269.

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Epilepsy is a chronic neurological disorder caused by abnormal neuronal activity that is diagnosed visually by analyzing electroencephalography (EEG) signals. Background: Surgical operations are the only option for epilepsy treatment when patients are refractory to treatment, which highlights the role of classifying focal and generalized epilepsy syndrome. Therefore, developing a model to be used for diagnosing focal and generalized epilepsy automatically is important. Methods: A classification model based on longitudinal bipolar montage (LB), discrete wavelet transform (DWT), feature extraction techniques, and statistical analysis in feature selection for RNN combined with long short-term memory (LSTM) is proposed in this work for identifying epilepsy. Initially, normal and epileptic LB channels were decomposed into three levels, and 15 various features were extracted. The selected features were extracted from each segment of the signals and fed into LSTM for the classification approach. Results: The proposed algorithm achieved a 96.1% accuracy, a 96.8% sensitivity, and a 97.4% specificity in distinguishing normal subjects from subjects with epilepsy. This optimal model was used to analyze the channels of subjects with focal and generalized epilepsy for diagnosing purposes, relying on statistical parameters. Conclusions: The proposed approach is promising, as it can be used to detect epilepsy with satisfactory classification performance and diagnose focal and generalized epilepsy.

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Gubanova, N. B., and Yu V. Karakulova. "Pathogenical meaning of serotoninergic mechanisms in the development of idiopatic generalised forms of epilepsy." Bulletin of Siberian Medicine 7, no. 5-1 (December 30, 2008): 87–89. http://dx.doi.org/10.20538/1682-0363-2008-5-1-87-89.

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Neurotransmitters disturbances with the certain role of serotoninergic system are in the basis of pathogenesis of epilepsy. 46 patients (29 females, 17-males) with idiopatic generalized epilepsy (mean age 21,8 ± 1,82) were investigated. In 30,4% of patients depressive disorders were revealed. Significant decreasing of blood serotonin level in patients with during the interictal period which decreased more after the generalised convulsive and myoclonic seasures was found by the immune assay method.

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French, Jacqueline A. "Seizure Exacerbation by Antiepileptic Drugs." Epilepsy Currents 5, no. 5 (September 2005): 192–93. http://dx.doi.org/10.1111/j.1535-7511.2005.00061.x.

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Worsening of Seizures by Oxcarbazepine in Juvenile Idiopathic Generalized Epilepsies Gelisse P, Genton P, Kuate C, Pesenti A, Baldy-Moulinier M, Crespel A Epilepsia 2004;45:1282–1286 Purpose Several studies have shown that carbamazepine (CBZ) may aggravate idiopathic generalized epilepsy (IGE). Oxcarbazepine (OXC) is a new drug chemically related to CBZ. We report six cases of juvenile IGE with a clear aggravation by OXC. Methods We retrospectively studied all patients with IGE first referred to our epilepsy department between January 2001 and June 2003 and treated with OXC. Results During this period, six patients were identified. All had an aggravation of their epilepsy in both clinical and EEG activities. OXC had been used because of an incorrect diagnosis of focal epilepsy or generalized tonic–clonic seizures (GTCSs) of undetermined origin (no syndromic classification of the epilepsy). Before OXC, only one patient had experienced a worsening of seizures with an inadequate drug (carbamazepine; CBZ). Four had juvenile myoclonic epilepsy, one had juvenile absence epilepsy, and one had IGE that could not be classified into a precise syndrome. OXC (dosage range, 300–1,200 mg/day) was used in monotherapy in all of them except for one patient. Aggravation consisted of a clear aggravation of myoclonic jerks (five cases) or de novo myoclonic jerks (one case). Three patients had exacerbation of absence seizures. One patient had worsened dramatically and had absence status, and one had de novo absences after OXC treatment. The effects of OXC on GTCSs were less dramatic, with no worsening in frequency in three and a slight increase in three. Conclusions OXC can be added to the list of antiepileptic drugs that can exacerbate myoclonic and absence seizures in IGE.

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Larivière, Sara, Raúl Rodríguez-Cruces, Jessica Royer, Maria Eugenia Caligiuri, Antonio Gambardella, Luis Concha, Simon S. Keller, et al. "Network-based atrophy modeling in the common epilepsies: A worldwide ENIGMA study." Science Advances 6, no. 47 (November 2020): eabc6457. http://dx.doi.org/10.1126/sciadv.abc6457.

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Epilepsy is increasingly conceptualized as a network disorder. In this cross-sectional mega-analysis, we integrated neuroimaging and connectome analysis to identify network associations with atrophy patterns in 1021 adults with epilepsy compared to 1564 healthy controls from 19 international sites. In temporal lobe epilepsy, areas of atrophy colocalized with highly interconnected cortical hub regions, whereas idiopathic generalized epilepsy showed preferential subcortical hub involvement. These morphological abnormalities were anchored to the connectivity profiles of distinct disease epicenters, pointing to temporo-limbic cortices in temporal lobe epilepsy and fronto-central cortices in idiopathic generalized epilepsy. Negative effects of age on atrophy further revealed a strong influence of connectome architecture in temporal lobe, but not idiopathic generalized, epilepsy. Our findings were reproduced across individual sites and single patients and were robust across different analytical methods. Through worldwide collaboration in ENIGMA-Epilepsy, we provided deeper insights into the macroscale features that shape the pathophysiology of common epilepsies.

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Suller Marti, AS, SM Mirsattari, KW MacDougall, D. Steven, A. Parrent, A. Andrade, S. de Ribaupierre, DC Diosy, R. McLachlan, and JG Burneo. "A.6 Vagus Nerve Stimulation in patients with therapy resistant generalized epilepsy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 48, s3 (November 2021): S15. http://dx.doi.org/10.1017/cjn.2021.268.

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Background: For patients with generalized epilepsy who do not respond to anti-seizure medications, the therapeutic options are limited. Vagus nerve stimulation (VNS) is a treatment mainly approved for therapy resistant focal epilepsy. There is limited information on the use of VNS on generalized epilepsies, including Lennox Gastaut Syndrome(LGS) and genetic generalized epilepsy(GGE). Methods: We identified patients with a diagnosis of Lennox-Gastaut Syndrome or Genetic Generalized Epilepsy, who underwent VNS implantation, between1997 and July 2018. Results: A total of 46 patients were included in this study with a history of therapy resistant generalized epilepsy. The mean age at implantation was 24 years(IQR= 17.8-31 years) and 50%(n=23) were female. The most common etiologies were GGE in 37%(n=17) and LGS in 63%(n=29). Median follow-up since VNS implantation was 63 months(IQR:31-112.8months). 41.7%(n=12) of the LGS group became responders, and 64.7%(n=11) in the GGE group. The best response in seizure reduction was seen in generalized tonic-clonic seizures. There was a reduction of seizure-related hospital admissions from 89.7%(N=26) pre-implantation, to 41.4%(N=12) post-implantation (p<0.0001). The frequency of side effects due to the stimulation was similar in both groups(62.1% in LGS and 61.1% in GGE). Conclusions: VNS is an effective treatment in patients with therapy resistant generalized epilepsy, especially GGE.

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Gilliam, F., B. J. Steinhoff, H. J. Bittermann, R. Kuzniecky, E. Faught, and B. Abou-Khalil. "Adult myoclonic epilepsy: A distinct syndrome of idiopathic generalized epilepsy." Neurology 55, no. 7 (October 10, 2000): 1030–33. http://dx.doi.org/10.1212/wnl.55.7.1030.

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Yakovleva, K. D., E. A. Kantemirova, and D. V. Dmitrenko. "Problems of diagnosing focal cortical dysplasia." Epilepsy and paroxysmal conditions 13, no. 1 (April 23, 2021): 33–43. http://dx.doi.org/10.17749/2077-8333/epi.par.con.2021.047.

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Focal cortical dysplasia (FCD) is one of the most common causes in developing pharmacoresistant epilepsy. We present the clinical case of the patient with generalized seizures. Routine electroencephalography (EEG) data registered diffuse epileptiform activity that allowed to diagnose genetic eneralized epilepsy and pharmacoresistant course of seizures.After performing magnetic resonance imaging using the epileptological program and video-EEG-monitoring, the diagnosis was revised: structural focal epilepsy with seizures with focal onset with oroalimentary, gesture automatisms in the right hand, bilateral tonic-clonic, uncompensated by levetiracetam monotherapy (1500 mg/day). Background disease: congenital malformation of the brain: FCD in the basal parts of the left temporal lobe. Lacosamide was added to the therapy in the drug dose 300 mg/day, and the frequency of epileptic seizures decreased. Differential diagnosis between genetic generalized epilepsy and structural epilepsy with FCD usually poses no obstacles. However, in some cases, structural epilepsy occurs under the “mask” of generalized epilepsy. Hence, this clinical case demonstrates the importance of diagnostic measures in the differential diagnostics of various forms of epilepsy to determine further tactics of patient management.

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Gansaeuer, M., and T. M. Alsaadi. "Carbamazepine-Induced Seizures: A Case Report and Review of the Literature." Clinical Electroencephalography 33, no. 4 (October 2002): 174–77. http://dx.doi.org/10.1177/155005940203300408.

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Carbamazepine has been reported to exacerbate seizures in children with primary generalized epilepsy and epilepsy with mixed seizure types. Seizure exacerbation has been rarely observed in adults, mainly in the mentally retarded or in those with primary generalized epilepsy. We present an adult patient who had frequent absence seizures and simple partial seizures for 20 years. She was treated with carbamazepine for over 16 years. The patient's EEG showed generalized spike and wave complexes. Her seizures remitted and the EEG normalized after the discontinuation of carbamazepine therapy.

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Liik, Maarika, Liina Vahter, Katrin Gross-Paju, and Sulev Haldre. "Cognitive Profile and Depressive Symptoms in Patients With Epilepsy." Medicina 49, no. 6 (June 4, 2013): 41. http://dx.doi.org/10.3390/medicina49060041.

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Background and Objective. The aim of the present study was to describe the cognitive profile of patients with focal and generalized epilepsy syndrome in comparison with healthy control subjects and to investigate whether depression was related to neuropsychological functioning in these patients. Material and Methods. A total of 36 patients with focal epilepsy and 26 patients with generalized epilepsy were compared with the control group of healthy volunteers (n=53). A battery of neuropsychological tests assessing verbal and visual spatial memory and executive functioning was carried out in addition to the completion of the Beck Depression Inventory (BDI). Results. The results indicated that patients with epilepsy performed significantly worse than controls on all verbal memory subscales and verbal fluency domains. The patients with focal epilepsy scored significantly worse than the patients with generalized epilepsy. The BDI scores were significantly correlated with several scores of the cognitive test in both patients’ groups but not in the control group. Conclusions. Our results suggest that patients with epilepsy, especially with focal-onset epilepsy, show cognitive disturbances predominantly in the verbal memory domain. In addition, depression was found to have a negative effect on cognitive functioning in patients with epilepsy.

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Ilyas, Mohammed, and Uğur Işık. "Focal versus Generalized Epilepsy—An Enigma." Journal of Pediatric Epilepsy 10, no. 02 (March 23, 2021): 043–44. http://dx.doi.org/10.1055/s-0041-1725992.

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Millichap, J. Gordon. "Generalized Epilepsy and Febrile Seizures Syndrome." Pediatric Neurology Briefs 13, no. 1 (January 1, 1999): 1. http://dx.doi.org/10.15844/pedneurbriefs-13-1-1.

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Patel, Shivali, and Mauran Sivananthan. "Compulsivity in Intractable Idiopathic Generalized Epilepsy." Journal of the Academy of Consultation-Liaison Psychiatry 63, no. 2 (March 2022): 180–81. http://dx.doi.org/10.1016/j.jaclp.2021.09.004.

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Mukhin, K. Yu. "Treatment priorities for idiopathic generalized epilepsy." Epilepsy and paroxysmal conditions 13, no. 1S (July 13, 2021): 71–73. http://dx.doi.org/10.17749/2077-8333/epi.par.con.2021.082.

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The report presents the current principles of treatment of various types of epileptic seizures and forms of epilepsy. High efficacy and good tolerability in mono- and combination therapy with lamotrigine are shown, including its beneficial effects on cognitive function, behavior, and mood in children.

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Journal articles on the topic 'Generalized Epilepsy'

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