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1

Rating, D. "SS-2-4 Therapeutic strategies in childhood epilepsis with special emphasis on intractable epilepsies in infants." Electroencephalography and Clinical Neurophysiology/Electromyography and Motor Control 97, no. 4 (September 1995): S67. http://dx.doi.org/10.1016/0924-980x(95)92659-a.

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2

Bahder, Brian W., Susan Halbert, De-Fen Mou, Ericka E. Helmick, Noemi Soto, Miriel Otero, and Alejandro E. Segarra. "Establishment of the Sea Grape Flatid, Petrusa epilepsis (Hemiptera: Fulgoroidea: Flatidae), in Florida." Florida Entomologist 101, no. 4 (December 1, 2018): 634. http://dx.doi.org/10.1653/024.101.0427.

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3

Anužytė, J. S., G. Rutkauskaitė, and R. Mameniškienė. "Tranzitorinė epilepsinė amnezija." Neurologijos seminarai 22, no. 77 (January 14, 2019): 213–18. http://dx.doi.org/10.29014/ns.2018.26.

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Tranzitorinė epilepsinė amnezija yra suaugusiųjų amžiuje prasidedančios temporalinės epilepsijos forma, kuri pasireiškia pasikartojančiais atminties sutrikimo epizodais. Pirmasis tranzitorinės epilepsinės amnezijos atvejis aprašytas daugiau kaip prieš šimtą metų, tačiau plačiau nagrinėti šį sutrikimą pradėta neseniai. Diagnozei patvirtinti taikomi 1998 m. suformuluoti kriterijai: 1) pasikartojantys liudininkų patvirtinti tranzitorinės amnezijos epizodai; 2) kitos pažinimo funkcijos epizodo metu nesutrikusios; 3) epilepsijos diagnozė paremta vienu ar daugiau iš pateiktų kriterijų: a) epilepsiforminis aktyvumas (EA) miego ir (arba) būdravimo elektroencefalogramoje (EEG); b) kiti epilepsijos priepuoliai (jeigu jų pradžia ir (ar) pasikartojimas yra susiję su tranzitorinės amnezijos epizodu); c) ryškus teigiamas vaistų nuo epilepsijos poveikis. Literatūroje nagrinėjami atvejai leidžia apibendrinti klinikinius simptomus: tranzitorine epilepsine amnezija suserga vidutinio amžiaus žmonės, dažniau – vyrai; amnezijos epizodai trumpi, linkę kartotis ir dažniau ištinka tik prabudus iš miego; atminties sutrikimui būdinga mišri anterogradinė ir retrogradinė amnezijos; 65 % pacientų amneziją lydi skonio ar kvapo haliucinacijos, déjà vu jausmas, trumpo nereagavimo epizodai, automatizmai; 43 % pacientų elektroencefalogramoje registruojami epilepsiforminiai potencialai temporalinėse skiltyse; įprastai tranzitorinės epilepsinės amnezijos priepuoliai nebesikartoja vartojant net mažas vaistų nuo epilepsijos dozes, tačiau tarp priepuolių gali išlikti paspartėjęs naujos informacijos užmiršimas, tolimos atminties praradimas ir topografinės atminties sutrikimas. Tranzitorinės epilepsinės amnezijos diferencinė diagnostika yra plati, neretai diagnozuojama netiksliai ir pavėluotai.
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4

Avanzini, Giuliano. "Do Seizures Promote Epileptogenesis and Cause Cognitive Decline?" European Neurological Review 9, no. 2 (2015): 120. http://dx.doi.org/10.17925/enr.2014.09.02.120.

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The assumption that repeated seizures may induce a progression of epilepsies towards an intractable condition and a cognitive decline does not hold true for idiopathic epilepsies but can only be considered for mesial temporal lobe epilepsy and epileptic encephalopathies. The available evidence leads to the conclusion that in most cases the epilepsy worsening and cognitive decline are due to the progression of the underlying pathology or to its interference with the developmental programme, the notable exception being the epileptic encephalopathies with continuous epileptic activity during sleep.
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5

Sukhov, A. A. "To the clinic "epilepsiae gastricae"." Neurology Bulletin XVIII, no. 1 (July 6, 2021): 177–84. http://dx.doi.org/10.17816/nb70828.

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Among the various forms of epileptic development, a clinical group of cases of epilepsy stands out, which some authors call epilepsia gastrica. The genesis and even the ethiology of this group is foggy, and only the clinical picture of epilepsy makes us agree to the temporary allocation of these cases to the epilepsia gastrica group.
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6

Matonytė, R., S. Ročka, and J. Grikinienė. "Vaikų epilepsijos gydymas kaliozotomija: du klinikiniai atvejai ir literatūros apžvalga." Neurologijos seminarai 24, no. 85 (December 29, 2020): 241–52. http://dx.doi.org/10.29014/ns.2020.32.

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Epilepsija yra viena iš dažniausių lėtinių vaikų ligų. Aktyvios vaikų epilepsijos paplitimas Lietuvoje, 2018 m. duomenimis, – 6,1/1000 vaikų. Nauji epilepsijos atvejai dažniausiai nustatomi vaikų arba vyresnių žmonių populiacijose. Epilepsija yra daugiaetiologinė liga ir pasireiškia labai įvairiais epilepsijos priepuoliais, kurių suvaldymas yra svarbiausias siekis gydant epilepsiją. Neslopinami priepuoliai gali sukelti vaiko kalbos, pažintinių funkcijų ir elgesio raidos sutrikimus – epilepsinę encefalopatiją. Veiksmingas epilepsijos gydymas vaikams ne tik pagerina sveikatos būklę, bet ir mažina socialinę atskirtį bei padeda integruotis į edukacinę veiklą. Tačiau, net ir anksti diagnozavus ligą ir paskyrus tinkamą gydymą vaistais nuo epilepsijos, epilepsijos priepuoliai išlieka 20-40 % sergančiųjų. Tokiems pacientams gali būti veiksmingas chirurginis epilepsijos gydymas – rezekcinės arba funkcinės (paliatyviosios) operacijos. Rezekcinis gydymas pagrįstas prielaida, kad epileptogeninės zonos pašalinimas apsaugo nuo priepuolių. Deja, kai kuriais atvejais epileptogeninė zona išlieka neaiški net ir po daugelio galvos smegenų tyrimų arba nesutampa su anatominio pažeidimo zona. Tokiu atveju rezekcinė operacija negali būti pritaikyta. Vienas iš veiksmingų sunkiai gydomos epilepsijos priepuolių kontrolės būdų yra paliatyvi chirurginė operacija – kaliozotomija (didžiosios smegenų jungties (corpus callosum) perpjovimas). Didžioji smegenų jungtis yra svarbiausia jungtis nerviniam impulsui plisti tarp abiejų smegenų pusrutulių, todėl jos atjungimas sutrikdo impulso plitimą tarp pusrutulių, taip sustabdydamas priepuolio generalizaciją. Klinikinių tyrimų duomenimis, kaliozotomija yra veiksminga iki 80-90 % operuotų pacientų – priepuoliai išnyksta arba reikšmingai sumažėja jų dažnis ir sunkumas. Aprašomi du pediatriniai pacientai, gydyti Vilniaus universiteto ligoninės Santaros klinikų Vaikų neurologijos ir neurochirurgijos skyriuose, kuriems buvo atlikta kaliozotomija ir palyginamos šių klinikinių atvejų išeitys su naujausių klinikinių tyrimų rezultatais.
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7

Shellhaas, Renée A., Courtney J. Wusthoff, Tammy N. Tsuchida, Hannah C. Glass, Catherine J. Chu, Shavonne L. Massey, Janet S. Soul, Natrujee Wiwattanadittakun, Nicholas S. Abend, and Maria Roberta Cilio. "Profile of neonatal epilepsies." Neurology 89, no. 9 (July 21, 2017): 893–99. http://dx.doi.org/10.1212/wnl.0000000000004284.

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Objective:Although individual neonatal epilepsy syndromes are rare, as a group they represent a sizable subgroup of neonatal seizure etiologies. We evaluated the profile of neonatal epilepsies in a prospective cohort of newborns with seizures.Methods:Consecutive newborns with seizures were enrolled in the Neonatal Seizure Registry (an association of 7 US children's hospitals). Treatment and diagnostic testing were at the clinicians' discretion. Neonates with seizures related to epileptic encephalopathies (without structural brain abnormalities), brain malformations, or benign familial epilepsies were included in this analysis.Results:Among 611 consecutive newborns with seizures, 79 (13%) had epilepsy (35 epileptic encephalopathy, 32 congenital brain malformations, 11 benign familial neonatal epilepsy [BFNE], 1 benign neonatal seizures). Twenty-nine (83%) with epileptic encephalopathy had genetic testing and 24/29 (83%) had a genetic etiology. Pathogenic or likely pathogenic KCNQ2 variants (n = 10) were the most commonly identified etiology of epileptic encephalopathy. Among 23 neonates with brain malformations who had genetic testing, 7 had putative genetic etiologies. Six infants with BFNE had genetic testing; 3 had pathogenic KCNQ2 variants and 1 had a pathogenic KCNQ3 variant. Comorbid illnesses that predisposed to acute symptomatic seizures occurred in 3/35 neonates with epileptic encephalopathy vs 10/32 with brain malformations (p = 0.03). Death or discharge to hospice were more common among newborns with brain malformations (11/32) than those with epileptic encephalopathy (3/35, p = 0.01).Conclusions:Neonatal epilepsy is often due to identifiable genetic causes. Genetic testing is now warranted for newborns with epilepsy in order to guide management and inform discussions of prognosis.
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8

Stanojlovic, Olivera, and Dragana Zivanovic. "Experimental models of epilepsy." Medical review 57, no. 7-8 (2004): 359–62. http://dx.doi.org/10.2298/mpns0408359s.

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Introduction An epileptic seizure is a clinical event and epilepsy is rather a group of symptoms than a disease. The main features all epilepsies have in common include: spontaneous occurrence, repetitiveness, and ictal correlation within the EEG. Epilepsies are manifested with distinct EEG changes, requiring exact clinical definition and consequential treatment. Current data show that 1% of the world's population (approximately 50 million people) suffers from epilepsy, with 25% of patients being refractory to therapy and requiring search for new substances in order to decrease EEG and behavioral manifestations of epilepsies. Material and methods In regard to discovery and testing of anticonvulsant substances the best results were achieved by implementation of experi- mental models. Animal models of epilepsy are useful in acquiring basic knowledge regarding pathogenesis, neurotransmitters (glutamate), receptors (NMDA/AMPA/kainate), propagation of epileptic seizures and preclinical assessment of antiepileptics (competitive and non-competitive NMDA antagonists). Results and conclusions In our lab, we have developed a pharmacologic model of a (metaphit, NMDA and remacemide-cilastatin) generalized, reflex, and audiogenic epilepsy. The model is suitable for testing various anticonvulsant substances (e.g. APH, APV, CPP, Mk-801) and potential antiepileptics (e.g. DSIP, its tetra- and octaanalogues).
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9

Halász, Péter. "Are Absence Epilepsy and Nocturnal Frontal Lobe Epilepsy System Epilepsies of the Sleep/Wake System?" Behavioural Neurology 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/231676.

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System epilepsy is an emerging concept interpreting major nonlesional epilepsies as epileptic dysfunctions of physiological systems. I extend here the concept of reflex epilepsy to epilepsies linked to input dependent physiological systems. Experimental and clinical reseach data were collected to create a coherent explanation of underlying pathomechanism in AE and NFLE. We propose that AE should be interpreted as epilepsy linked to the corticothalamic burst-firing mode of NREM sleep, released by evoked vigilance level oscillations characterized by reactive slow wave response. In the genetic variation of NFLE the ascending cholinergic arousal system plays an essential role being in strong relationship with a gain mutation of the nicotinic acethylcholin receptors, rendering the arousal system hyperexcitable. I try to provide a more unitary interpretation for the variable seizure manifestation integrating them as different degree of pathological arosuals and alarm reactions. As a supporting hypothesis the similarity between arousal parasomnias and FNLE is shown, underpinned by overlaping pathomechanism and shared familiarity, but without epileptic features. Lastly we propose that both AE and NFLE are system epilepsies of the sleep-wake system representing epileptic disorders of the antagonistic sleep/arousal network. This interpretation may throw new light on the pathomechanism of AE and NFLE.
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10

Zubkov, Sarah, and Ruben Kuzniecky. "Genetic Advances in Epilepsy." US Neurology 11, no. 02 (2015): 96. http://dx.doi.org/10.17925/usn.2015.11.02.96.

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Approximately 40–70 % of all epilepsies are now estimated to have a genetic cause. Though most epilepsies are genetically complex, the past decade has seen an explosion of advances in genetic etiologies. Early gene discovery in epilepsy was limited to large families with milder, inherited monogenic epilepsies using linkage analysis. Newer techniques underlie the past decade’s accelerated gene discovery, especially in noninherited, severe epileptic encephalopathies, and have reinforced the diverse role of cellular functions that may be affected. This review examines recently discovered epilepsy genes and discusses the importance of a genetic diagnosis in patient care.
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11

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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12

Rangarajan, Punitha, Kulandaiammal Moorthy, and Arunan Subbiah. "Observational study on the utilization pattern of adjuvant anti-epileptics and their adverse effects." International Journal of Basic & Clinical Pharmacology 9, no. 1 (December 24, 2019): 170. http://dx.doi.org/10.18203/2319-2003.ijbcp20195781.

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Background: Epilepsy is a disease characterized by an enduring predisposition to generate epileptic seizures. Pharmacological therapy is the cornerstone of treatment of epilepsy. In more than 50% patients seizure not controlled with first-line anti-epileptic drugs so added with adjuvant drugs. Therefore adjuvant anti-epileptic drugs play an important role in preventing seizure remission in known epilepsy patients. Observational study was to evaluate the utilisation pattern of adjuvant anti-epileptic drugs and to assess their clinical correlation and observe the adverse effects of the adjuvant anti-epileptics.Methods: Eligible 100 patients who attended the neurology outpatient department where enrolled in the study. Demographic data, type of epilepsy, presence or absence of seizure episode (4 months), adjuvant anti-epileptic prescribed along with the first-line drugs and adverse effects were noted. Clinical correlation and rationale for the usage of adjuvant anti-epileptics were assessed. Descriptive statistics used for statistical analysis.Results: The most common types of seizures were generalised tonic clonic seizures (41%) and complex partial seizures (37%). Most commonly used 1st line drug was phenytoin tablet. Most common adjuvant anti-epileptics used were clonazepam (30), clobazam (24) tablets. Most common adverse effect noted was dizziness (31%).Conclusions: Tablet clonazepam is effective adjunct for tonic clonic seizures. Clobazam table is recommended as add-on drug for focal and generalised seizures. Adjuvant anti-epileptic drugs decrease seizure remission with fewer tolerable adverse effects.
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Møller, Rikke S., Thomas V. Wuttke, Ingo Helbig, Carla Marini, Katrine M. Johannesen, Eva H. Brilstra, Ulvi Vaher, et al. "Mutations in GABRB3." Neurology 88, no. 5 (January 4, 2017): 483–92. http://dx.doi.org/10.1212/wnl.0000000000003565.

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Objective:To examine the role of mutations in GABRB3 encoding the β3 subunit of the GABAA receptor in individual patients with epilepsy with regard to causality, the spectrum of genetic variants, their pathophysiology, and associated phenotypes.Methods:We performed massive parallel sequencing of GABRB3 in 416 patients with a range of epileptic encephalopathies and childhood-onset epilepsies and recruited additional patients with epilepsy with GABRB3 mutations from other research and diagnostic programs.Results:We identified 22 patients with heterozygous mutations in GABRB3, including 3 probands from multiplex families. The phenotypic spectrum of the mutation carriers ranged from simple febrile seizures, genetic epilepsies with febrile seizures plus, and epilepsy with myoclonic-atonic seizures to West syndrome and other types of severe, early-onset epileptic encephalopathies. Electrophysiologic analysis of 7 mutations in Xenopus laevis oocytes, using coexpression of wild-type or mutant β3, together with α5 and γ2s subunits and an automated 2-microelectrode voltage-clamp system, revealed reduced GABA-induced current amplitudes or GABA sensitivity for 5 of 7 mutations.Conclusions:Our results indicate that GABRB3 mutations are associated with a broad phenotypic spectrum of epilepsies and that reduced receptor function causing GABAergic disinhibition represents the relevant disease mechanism.
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14

Yin, Jianing. "Research on the Direction of Ion Channel Related to Epileptic Seizures." E3S Web of Conferences 218 (2020): 03013. http://dx.doi.org/10.1051/e3sconf/202021803013.

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Epilepsy is a group of chronic brain diseases characterized by transient central nervous system dysfunction caused by repeated abnormal synchronization of neuronal discharges in the brain, with sudden onset and repeated seizures. Epilepsy has been listed as one of the five major neuropsychiatric diseases of the World Health Organization (WHO). Hereditary epilepsy refers to epilepsy syndromes previously classified as idiopathic generalized epilepsies (IGEs), which encompasses several different epilepsy syndromes ranging in clinical severity from relatively benign febrile convulsions (FS) and childhood absence epilepsy (CAE) to the more severe juvenile myoclonic epilepsy (JME) and generalized epileptic seizures with febrile convulsions (GEFS+). This article analyzes the direction of ion channel related to epileptic seizures. It will look forward to the future research direction of some of the ion channels related to epileptogenesis.
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Malik, Roopa, Viral Kumar, Susheela Chaudhary, and Nirmala Duhan. "Obstetric and neonatal outcome in women with epilepsy." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 6, no. 6 (May 25, 2017): 2593. http://dx.doi.org/10.18203/2320-1770.ijrcog20172358.

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Background: Epilepsy is the second most common neurological disorder complicating pregnancy next to migraine. Both mother and fetus stay at risk due to epilepsy and side effects of antiepileptic’s. This retrospective study was conducted to study fetal and maternal outcome in WWE.Methods: This study was conducted on 55 patients of epilepsy with pregnancy who attended antenatal clinic of our hospital from January 2016 to December 2016. Data was collected using antenatal registers in outdoor settings and medical case sheets in indoor patients and was analyzed statistically.Results: There were a total of 55 WWE in one year duration. Incidence of epilepsy being 0.4% in this study. 11 WWE were not on ante epileptic drug when conceived, while 34 WWE were on ante epileptic drugs when conceived, 8 WWE were newly diagnosed and 2 patients had both psychiatric disorders along with epilepsy. There were 3 IUDs, 4 major congenital malformation and 2 minor malformations. 2 major malformation occurred in patients taking both antipsychotic and ante epileptics since conception.Conclusions: There were a total of 55 WWE in one year duration. Incidence of epilepsy being 0.4% in this study. 11 WWE were not on ante epileptic drug when conceived, while 34 WWE were on ante epileptic drugs when conceived, 8 WWE were newly diagnosed and 2 patients had both psychiatric disorders along with epilepsy. There were 3 IUDs, 4 major congenital malformation and 2 minor malformations. 2 major malformation occurred in patients taking both antipsychotic and ante epileptics since conception.
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Devinsky, Orrin. "Is Behavior in Temporal Lobe Epilepsy Different than in Other Epilepsies? the Jury is Out." Epilepsy Currents 7, no. 4 (July 2007): 95–96. http://dx.doi.org/10.1111/j.1535-7511.2007.00184.x.

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Interictal Depression, Anxiety, Personality Traits, and Psychological Dissociation in Patients with Temporal Lobe Epilepsy (TLE) and Extra-TLE. Swinkels WA, van Emde Boas W, Kuyk J, van Dyck R, Spinhoven P. Epilepsia 2006;47(12):2092–2103. PURPOSE: This study was performed to investigate the relation between symptoms of interictal depression, anxiety, personality traits, and psychological dissociation with the localization and lateralization of the epileptogenic zone in patients with partial epilepsy. METHODS: All patients were diagnosed according to the localization-related concept of the 1989 International League Against Epilepsy (ILAE) Classification of Epilepsies and Epileptic Syndromes, and the localization and lateralization of the epileptogenic zone was established by using the clinical criteria for noninvasive presurgical evaluation. This resulted in 67 patients with temporal lobe epilepsy (TLE) and 64 patients with extra-TLE. All patients were assessed on the various aspects of psychopathology by using a comprehensive battery of standardized diagnostic instruments. RESULTS: We did not find the hypothesized excess of psychiatric symptoms in patients with (mesial) TLE in comparison with patients with extra-TLE. We also found no differences between patients with the lateralization of epilepsy in the left versus the right hemisphere. CONCLUSIONS: TLE per se cannot be considered a risk factor in developing more or more severe symptoms of psychopathology in patients with partial epilepsy. Concomitant factors, such as the duration of epilepsy, seizure frequency, and frontal lobe dysfunction may play an additional role. Our findings support the hypothesis of a multifactorial explanation for the psychiatric symptoms in patients with epilepsy.
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Kravljanac, Ruzica, and Milena Djuric. "Childhood epileptic seizures imitating migraine and encephalitis." Srpski arhiv za celokupno lekarstvo 140, no. 9-10 (2012): 558–62. http://dx.doi.org/10.2298/sarh1210558k.

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Introduction. Paroxismal events can resemble epileptic seizures, however, some epileptic seizures, especially benign occipital childhood epilepsies can imitate migraine, cycling vomiting or encephalitis. Objective. The aim of this study was evaluation of clinical and electroencephalographic (EEG) features and outcome in children with benign occipital childhood epilepsies. Methods. Investigation included 18 patients with benign occipital childhood epilepsies hospitalized in the period from 2007 to 2010. The diagnosis was based on clinical and EEG characteristics of seizures, while treatment included acute therapy for seizures and chronic antiepileptic drugs. Prognosis was analyzed in terms of neurological outcome and seizure recurrence rate. Results. Benign occipital childhood epilepsy with early onset was diagnosed in 15 children. Vegetative symptoms, mostly ictal vomiting (13), eye deviation and loss of consciousness (13) dominated in the clinical presentation. The most frequent EEG findings showed occipital epileptic discharges. Benign occipital childhood epilepsy with late onset was diagnosed in three cases. Seizures were manifested by visual hallucinations, headache and secondary generalized convulsions. All three patients were administered chronic antiepileptic drugs and had good outcome. Conclusion. In our patients, clinical manifestations of benign occipital epilepsies had some similarities with clinical features of migraine and encephalitis. It could explain misdiagnosis in some of them. Knowledge about main features and differences between each of these disorders is crucial for making appropriate diagnosis.
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Appleton, Richard E., Amanda Freeman, and J. Helen Cross. "Diagnosis and management of the epilepsies in children: a summary of the partial update of the 2012 NICE epilepsy guideline." Archives of Disease in Childhood 97, no. 12 (October 6, 2012): 1073–76. http://dx.doi.org/10.1136/archdischild-2012-302822.

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The epilepsies of childhood are a heterogeneous group of disorders with different causes, treatments and outcomes. The choice of anti-epileptic drug is largely determined by its effectiveness in a specific epilepsy syndrome, or seizure type(s) if a syndrome cannot be readily identified, and the drug's safety profile. There are minimal randomised controlled trial data to help inform this decision. In January 2012, the National Institute for Health and Clinical Excellence (NICE) published its partially revised and updated clinical guideline on the pharmacological treatment of the epilepsies in children and adults. This partial update provides additional data and also specific recommendations that improve the evidence base for the use of specific anti-epileptic drugs in treating the epilepsies of childhood.
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Özer, Erdal, and Halis Dokgöz. "Epileptik Hastalarda Ani ve Beklenmedik Ölümlere Adli Tıp Yaklaşımı." Bulletin of Legal Medicine 9, no. 3 (December 1, 2004): 79–86. http://dx.doi.org/10.17986/blm.200493557.

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Epileptik hastanın tanık olunmuş veya olunmamış ani, beklenmedik bir biçimde travma ve suda boğulma ve status epileptikus dışı ölümü ve postmortem incelemede ölüm nedenine açıklık getirecek herhangi bir anatomik ve toksikolojik sebep tespit edilemediği durumlar epileptik hastalarda ani beklenmedik ölüm (EHABO) olarak değerlendirilmektedir. EHABÖ, uzun zamandır bilinmekte fakat epilepsili hastalardaki artmış mortalité her zaman kabul edilmemektedir. 1960'lı yıllarda epilepsi hastasının epileptik olmayan kadar uzun yaşamamasına hiçbir neden olmadığı düşünülmekteydi. EHABO, hala geniş çapta kabul görmemekte ve bu yüzden risk faktörlerini belirlemeye yönelik epidemiyolojik çalışmalar bu gibi engellere takılmaktadır. Epileptik hastadaki ani ölüm riskinin epileptik olmayan birine göre yaklaşık 24 kat fazla olduğu bildirilmektedir. EHABÖ, yüzyılın sonlarına doğru bildirilmişse de bu fenomenin insidansı ve patofizyolojisi tam olarak henüz anlaşılamamıştır. EHABÖ insidansı, olası mekanizmalar, potansiyel risk faktörleri ve araştırma yöntemleri derlenerek ülkemizdeki adli tıp uygulamaları açısından konu irdelenmiştir.Anahtar Kelimeler: Epilepsi, ani beklenmedik ölüm, adli tıp.
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Alam, Shouja, and Andrew L. Lux. "Epilepsies in infancy." Archives of Disease in Childhood 97, no. 11 (September 8, 2012): 985–92. http://dx.doi.org/10.1136/archdischild-2011-301119.

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To evaluate and manage epileptic seizures and other paroxysmal events in infants, it is necessary to ask five key questions: (1) Is this a type of epilepsy?; (2) What seizure type(s) are occurring?; (3) Do these seizure types, combined with factors such as age at onset and EEG features, constitute an ‘epilepsy syndrome’?; (4) What investigations do we need to do in searching for an underlying aetiology? and finally, (5) What is the prognosis for neurological and developmental state in later life?This review considers epilepsies that have an onset in infancy but after the perinatal period, outlines the commoner epilepsy syndromes occurring in this age group and describes paroxysmal events that can mimic epilepsy. Epilepsies in infancy may be the manifestation of a genetic predisposition associated with a benign course and good prognosis for neurodevelopment. In contrast, they may pose the challenging situation of ‘epileptic encephalopathy’, rare but potentially treatable metabolic conditions, or structural abnormalities with poor developmental outlook and intractable seizures. Seizures in infancy are relatively rare and there is a wide range of underlying causes, some of which require specific treatments to avoid preventable neurodevelopmental damage. Guidance from the National Institute for Health and Clinical Excellence suggests early referral of cases of infantile epilepsy to a tertiary centre.
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Zupanc, Mary L. "Clinical Evaluation and Diagnosis of Severe Epilepsy Syndromes of Early Childhood." Journal of Child Neurology 24, no. 8_suppl (August 2009): 6S—14S. http://dx.doi.org/10.1177/0883073809338151.

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The developing brain is particularly susceptible to seizures. Diffuse central nervous system pathology or injury in early infancy, when the brain is most vulnerable, may lead to catastrophic epilepsies such as Ohtahara's epileptic encephalopathy and early myoclonic epileptic encephalopathy. These epileptic encephalopathies are difficult to treat and have poor prognoses. As the brain undergoes programmed synaptogenesis, apoptosis, and myelination, the epilepsy phenotypes and electroencephalography (EEG) findings change, producing age-dependent epileptic encephalopathies. Specifically, as they grow older, 40% to 60% of infants with infantile spasms and a concomitant hypsarrhythmia on EEG will develop Lennox-Gastaut syndrome with tonic and atonic seizures, associated with a synchronous, generalized 1.5- to 2-Hz spike and slow wave discharges on EEG. In the context of age-dependent epileptic encephalopathies, as an epilepsy syndrome is evolving, it is often difficult to accurately diagnose the specific epilepsy syndrome in a young child who presents with seizures. It is the clinical evolution of the seizure types and the EEG that helps the clinician make an accurate diagnosis. As more is known about the underlying pathophysiology for the various epilepsy syndromes, not only the clinical picture and EEG but also a genetic blood test will be used to accurately diagnose a specific epilepsy syndrome. A case in point would be severe myoclonic epilepsy of infancy (classically known as Dravet syndrome) and severe myoclonic epilepsy of infancy-borderland/ borderline, which are associated with specific mutations in the sodium ion channel gene SCN1A.
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Deopa, Bindu, Bhawna Chaudhary, and Ashish Gupta. "An observational study to determine the status of serum and RBC folate in drug resistant epileptic children at a tertiary care centre in Western Rajasthan, India." International Journal of Contemporary Pediatrics 7, no. 7 (June 24, 2020): 1554. http://dx.doi.org/10.18203/2349-3291.ijcp20202615.

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Background: Drug resistant epilepsies constitute about 10-20% of childhood epilepsies and treated with higher doses and multiple AEDs. AEDs increases folate metabolism by enzyme induction thus causes deficiency of folic acid.Objective was to evaluate the effect on serum and RBC folate in children having drug resistant epilepsy.Methods: In a prospective observational study 83 drug resistant epileptic children of age 6months to 180 months fulfilled the inclusion criteria enrolled in study, from Oct 2014 to Nov 2016 for a period of two years. Serum and RBC folate levels were done in these children. Epileptic children already receiving folic acid supplementation/treatment were excluded from the study. Children with serum folate level <5ng/ml and RBC folate <280ng/ml was considered as folate deficiency.Results: Total 83 children had drug resistant epilepsy (defined by ILAE). Mean age of children with drug resistant epilepsy was 71.39±49.76 months. 71.08 % were male and 28.91% were female. Mean serum folate in these children was 7.75±2.77 ng/ml and RBC folate 381.63±164.54 ng/ml which was significantly lower as compared to healthy children or epileptic not receiving AEDs. 14.45 % children in drug resistant epilepsy had serum folate <5ng/ml while 20.89% were found to be RBC folate deficient (RBC level <280ng/ml).Conclusions: Antiepileptic drugs are associated with lower blood folate status which deteriorates further with increasing number and doses of AEDs in drug resistant patients. Therefore blood folate monitoring should be done in all children on AEDs on regular intervals and should be considered in the etiologic differentials of drug resistant epilepsy.
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Unalp, Aycan, Elcin Bora, Tufan Cankaya, Ozlem Giray Bozkaya, Derya Ercal, Aysel Ozturk, and Ayfer Ulgenalp. "Lack of Association of Childhood Partial Epilepsy with Brain Derived Neurotrophic Factor Gene." Scientific World Journal 2012 (2012): 1–5. http://dx.doi.org/10.1100/2012/414797.

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Brain-derived factor (BDNF) is a member of neurotrophin family and is localized and upregulated in areas implicated in epileptogenesis. Several lines of evidence make the BDNF gene a plausible candidate gene for predisposition to epilepsy. In this study, we tested that BDNF might be involved in the etiology of childhood PE. To assess whether BDNF gene C270T polimorphism could be implicated in vulnerability to PE, we conducted a case-control association analysis (112 partial epileptic and 100 controls) in Turkish children. Epileptic children were divided into two groups: 1—idiopathic (n=85) and 2—symptomathic epilepsy (n=27). There was no significant difference in genotypic distribution and allelic frequencies of the BDNF gene C270T polimorphism between the PE and control groups. However, the BDNF gene TT genotype was more frequently seen in the epileptic children (15 versus 11 patients, resp.). Interestingly, in the epilepsy group, both two children with TT genotype have posttraumatic epilepsy. The data indicate a possible association with the 270T genotype of the BDNF gene with a posttraumatic epilepsy. To draw any conclusion, further studies using larger sample sizes should be carried out in various ethnic populations in childhood epilepsies.
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Dulac, O. "Une epilepsie ? Des epilepsies ! : de la clinique a l’imagerie." Journal de Radiologie 85, no. 9 (September 2004): 1429. http://dx.doi.org/10.1016/s0221-0363(04)77397-7.

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Hebbar, Malavika, and Heather C. Mefford. "Recent advances in epilepsy genomics and genetic testing." F1000Research 9 (March 12, 2020): 185. http://dx.doi.org/10.12688/f1000research.21366.1.

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Developmental and epileptic encephalopathies (DEEs) are a group of severe, early onset epilepsies characterized by refractory seizures, developmental delay or regression associated with ongoing epileptic activity, and generally poor prognosis. DEE is genetically and phenotypically heterogeneous, and there is a plethora of genetic testing options to investigate the rapidly growing list of epilepsy genes. However, more than 50% of patients with DEE remain without a genetic diagnosis despite state-of-the-art genetic testing. In this review, we discuss the major advances in epilepsy genomics that have surfaced in recent years. The goal of this review is to reach a larger audience and build a better understanding of pathogenesis and genetic testing options in DEE.
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Wieser, Heinz Gregor. "Genetic epilepsies. Remarks on the proposed “Organization of the Epilepsies”." Journal of Epileptology 22, no. 1 (June 1, 2014): 11–23. http://dx.doi.org/10.1515/joepi-2015-0011.

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SUMMARYIntroduction.Genetic findings in several epilepsy syndromes provide insights into the pathophysiology of specific subtypes of epilepsy and into mechanisms of epileptogenesis, because the genes encoding ion channels, and proteins associated to the vesical synaptic cycle, or involved in energy metabolism, influence neuronal excitability.Aim.The following aspects of genetic epilepsies will be discussed: new proposed “organization of the epilepsies”, genetic and other etiologies, electroclinical syndromes and their genetics and genetic testing in the epilepsies.Methods.The updated review is based on OMIM™ (Online Mendelian Inheritance in Man).Review and remarks.Because of the vast genetic and phenotypic heterogeneity, bridging genotype and phenotype remains a major challenge in epilepsy genetics. The so-called “idiopathic” epilepsies are genetically determined. The new ILAE proposal on the “organization” of the epilepsies takes into account the genetic advances. However, despite proposed changes in the nomenclature, the concept of the electroclinical syndrome, i.e. seizure types, age-dependent onset, electroencephalographic criteria, and concomitant symptoms, such as movement disorders or developmental delay, remain important criteria to group the epilepsies. Although also the differentiation “generalized” versus “focal” is nowadays discussed critically, for practical reasons these categories remain valid. Similarly the categories “benign” syndromes of early childhood, epileptic encephalopathies, and fever-associated syndromes, have their utility.Conclusions.The large number of genetic defects in the epilepsies complicates their analysis. However, it is anticipated that novel genetic methods, that are able to analyze all known genes at a reasonable price, will help identify novel diagnostic and therapeutic avenues, including prognostic and genetic counseling. Today it is already possible to include into genetic testing genes responsible for the side effects of AEDs. In addition, for some epilepsy phenotypes it has became possible to predict the most efficacious antiepileptic drugs for patients based on their genetic makeup. Thus, the development of individualized medicine is expected to greatly improve the management of epilepsy patients.
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Deb, S., and David Hunter. "Psychopathology of People with Mental Handicap and Epilepsy I: Maladaptive Behaviour." British Journal of Psychiatry 159, no. 6 (December 1991): 822–26. http://dx.doi.org/10.1192/bjp.159.6.822.

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One hundred and fifty mentally handicapped people (100 from hospital and 50 from the community) with epilepsy were studied along with an individually matched control group of 150 (100 from hospital and 50 from the community) non-epileptic mentally handicapped people. Behaviour was studied using the Profile of Abilities and Adjustment Schedule. Of the total population, 55.3% showed some type of severe behaviour problem. Although the epileptics showed slightly more severe behaviour problems than the non-epileptic group, there was no statistically significant difference between the two groups. Some differences emerged between the groups when subgroups of epileptics were studied.
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Blume, Warren T. "Hyperventilation, More than Just Hot Air." Epilepsy Currents 6, no. 3 (May 2006): 76–77. http://dx.doi.org/10.1111/j.1535-7511.2006.00103.x.

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Hyperventilation Revisited: Physiological Effects and Efficacy on Focal Seizure Activation in the Era of Video-EEG Monitoring Guaranha MS, Garzon E, Buchpiguel CA, Tazima S, Yacubian EM, Sakamoto AC Epilepsia 2005;46(1):69–75 Purpose Hyperventilation is an activation method that provokes physiological slowing of brain rhythms, interictal discharges, and seizures, especially in generalized idiopathic epilepsies. In this study, we assessed its effectiveness in inducing focal seizures during video-EEG monitoring. Methods We analyzed the effects of hyperventilation (HV) during video-EEG monitoring of patients with medically intractable focal epilepsies. We excluded children younger than 10 years, mentally retarded patients, and individuals with frequent seizures. Results We analyzed 97 patients; 24 had positive seizure activation (PSA), and 73 had negative seizure activation (NSA). No differences were found between groups regarding sex, age, age at epilepsy onset, duration of epilepsy, frequency of seizures, and etiology. Temporal lobe epilepsies were significantly more activated than frontal lobe epilepsies. Spontaneous and activated seizures did not differ in terms of their clinical characteristics, and the activation did not affect the performance of ictal single-photon emission computed tomography (SPECT). Conclusions HV is a safe and effective method of seizure activation during monitoring. It does not modify any of the characteristics of the seizures and allows the obtaining of valuable ictal SPECTs. This observation is clinically relevant and suggests the effectiveness and the potential of HV in shortening the presurgical evaluation, especially of temporal lobe epilepsy patients, consequently reducing its costs and increasing the number of candidates for epilepsy surgery.
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Krayeva, L. S., and V. M. Alifirova. "Organization of children epileptological service in Tomsk Region." Bulletin of Siberian Medicine 7, no. 5-1 (December 30, 2008): 198–99. http://dx.doi.org/10.20538/1682-0363-2008-5-1-198-199.

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This article shows the analysis of working of the child epileptological room for 2002—2007. The goals of the room are determinate, the groups of the children, examined in the room and being registrating, are selected. Learning the example of 650 children with epilepsy, who are registrating, we found out the domination of focal symptomatic or probably symptomatic form (62,2%). Idiopathic generalized epilepsies made 13,3% with predominance of child absence epilepsies — 39,8%. Epileptic encephalopathy made 3,46% with predominance of West syndrome — 64,3%. In treatment monotherapy were used in 75% of cases, the polytherapy took 25%.
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Bayat, Allan, Michael Bayat, Guido Rubboli, and Rikke S. Møller. "Epilepsy Syndromes in the First Year of Life and Usefulness of Genetic Testing for Precision Therapy." Genes 12, no. 7 (July 8, 2021): 1051. http://dx.doi.org/10.3390/genes12071051.

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The high pace of gene discovery has resulted in thrilling advances in the field of epilepsy genetics. Clinical testing with comprehensive gene panels, exomes, or genomes are now increasingly available and have led to a significant higher diagnostic yield in early-onset epilepsies and enabled precision medicine approaches. These have been instrumental in providing insights into the pathophysiology of both early-onset benign and self-limited syndromes and devastating developmental and epileptic encephalopathies (DEEs). Genetic heterogeneity is seen in many epilepsy syndromes such as West syndrome and epilepsy of infancy with migrating focal seizures (EIMFS), indicating that two or more genetic loci produce the same or similar phenotypes. At the same time, some genes such as SCN2A can be associated with a wide range of epilepsy syndromes ranging from self-limited familial neonatal epilepsy at the mild end to Ohtahara syndrome, EIFMS, West syndrome, Lennox–Gastaut syndrome, or unclassifiable DEEs at the severe end of the spectrum. The aim of this study was to review the clinical and genetic heterogeneity associated with epilepsy syndromes starting in the first year of life including: Self-limited familial neonatal, neonatal-infantile or infantile epilepsies, genetic epilepsy with febrile seizures plus spectrum, myoclonic epilepsy in infancy, Ohtahara syndrome, early myoclonic encephalopathy, West syndrome, Dravet syndrome, EIMFS, and unclassifiable DEEs. We also elaborate on the advantages and pitfalls of genetic testing in such conditions. Finally, we describe how a genetic diagnosis can potentially enable precision therapy in monogenic epilepsies and emphasize that early genetic testing is a cornerstone for such therapeutic strategies.
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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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Krayeva, L. S., and V. M. Alifirova. "Clinical and epidemiological characteristic of epilepsy in children and teenagers in Tomsk Region." Bulletin of Siberian Medicine 9, no. 4 (August 28, 2010): 73–76. http://dx.doi.org/10.20538/1682-0363-2010-4-73-76.

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The incidence of epilepsy and epileptic syndromes (number of new cases per year in a given population) in children and teenagers of Tomsk Region was 44.10 per 100 000 people, being higher in children (49.60) as compared to teenagers (27.39). The prevalence (number of active cases per unit population) was 3.53 per 1 000 people and differs among regions (from 0.74 to 10.95). Most of patients suffered from symptomatic (45.58%) focal epilepsies with predominantly temporal lobe epilepsies (42.04%). The most common etiologic factors of symptomatic focal epilepsies were hypoxic-ischemic perinatal encephalopathies and developmental brain disorders (15.9%). 24.26% patients were switched to politherapy, and others — to monotherapy. Valproates were most often used drug. Remission was achieved in 49.43%.
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Ghossein, J., and D. Pohl. "P.052 Benign spasms of infancy - a mimicker of infantile epileptic disorders." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 46, s1 (June 2019): S28. http://dx.doi.org/10.1017/cjn.2019.152.

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Background: Benign spasms of infancy (BSI), previously described as benign non-epileptic infantile spasms or benign myoclonus of early infancy, are non-epileptic movements manifesting during the first year of life and spontaneously resolving in the second year of life. BSI are characterized by spasms typically lasting 1-2 seconds, involving to varying degrees the head, neck, trunk, shoulders and upper extremities. Ictal and interictal EEG recordings are normal. BSI are not associated with developmental retardation and do not require treatment. Distinction between BSI and infantile epileptic disorders, such as epileptic spasms or myoclonic epilepsy of infancy, can be challenging given the clinical similarities. Moreover, interictal EEGs can be normal in all conditions. Epileptic spasms and myoclonic epilepsy require timely treatment to improve neurodevelopmental outcomes. Methods: We describe a 6-month old infant presenting with spasm-like movements. His paroxysms as well as a positive family history for epileptic spasms were in keeping with a likely diagnosis of West syndrome. Results: Surprisingly, ictal video EEG did not reveal epileptiform activity, and suggested a diagnosis of BSI. Conclusions: We emphasize that ictal EEG is the gold standard for classification of infantile paroxysms as either epileptic or non-epileptic, thereby avoiding overtreatment of BSI and facilitating timely targeted treatment of infantile epilepsies.
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Darra, Francesca, Bernardo Bernardina, Natalio Fejerman, and Roberto Caraballo. "Clinical and EEG Features of Idiopathic Focal Epilepsies in Childhood." Journal of Pediatric Epilepsy 05, no. 03 (June 20, 2016): 116–21. http://dx.doi.org/10.1055/s-0036-1584669.

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The International League Against Epilepsy (ILAE) report lists three well-defined syndromes of idiopathic focal epilepsies in childhood: benign childhood epilepsy with centrotemporal spikes (BCECTS), Panayiotopoulos syndrome (PS), and idiopathic childhood occipital epilepsy of Gastaut (ICOE-G). The concept of idiopathic and benign focal epilepsies in childhood is relevant as the term implies absence of structural brain lesions and genetic predisposition in the presence of age-dependent seizures. BCECTS is the most frequent of the benign focal epilepsies in childhood accounting for 15 to 25% of epilepsy syndromes in children below 15 years of age. It is also the most frequent epilepsy syndrome occurring at school age. The prevalence of PS was around 13% in children aged 3 to 6 years with one or more nonfebrile seizures, and 6% in the age group of 1 to 15 years. These figures may be higher if children who are currently considered to have an atypical clinical presentation are included in the syndrome. PS is the most common specific cause of nonfebrile status epilepticus in childhood. ICOE “Gastaut type” is a rare manifestation of a focal idiopathic epilepsy that has an age-related onset and is often age limited. The seizures of ICOE Gastaut type are always of occipital-lobe onset and primarily manifest with visual seizures, which are the most typical and usually the first ictal symptom, but other types of seizures may be associated. ICOE “Gastaut type” is a rare condition with a probable prevalence of 0.2 to 0.9% of all epilepsies, and accounting for 2 to 7% of benign childhood focal seizures.The recognition of these age-dependent epileptic syndromes is crucial for the adequate management of the children and their family.
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Arbune, Anca Adriana, Oana Tarta Arsene, Lacramioara Brinduse, and Dana Craiu. "EPILEPTIC SEIZURE TRIGGERS IN CHILDREN FROM ROMANIA." Romanian Journal of Neurology 15, no. 2 (June 30, 2016): 80–85. http://dx.doi.org/10.37897/rjn.2016.2.5.

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Objectives. The identification of the types, characteristics and correlations of epileptic seizure triggers in children with epilepsy from Romania. Material and methods. Transversal observational study on 278 children with epilepsy using the questionnaire method, containing questions regarding seizure characteristics, demographical information and medical history. Results. The lot characteristics were average age 9.74 years; 57.2% males; 19.4% positive epilepsy family history; 48.2% late psychomotor development; 54% deficitary neuropsychological development; 25.2% treatment resistant epilepsies; 59.7% of children had focal epileptic seizures, 35.3% had generalized. Average number of triggering factors was 3 and 20.1% of children had no seizure trigger. The most frequently reported factors were: sleep deprivation 39.57%, anxiety 23%, sleep disturbances 22.66%, fever 20.50%, anger 19%, light stimulation 17.27%, crying 16.19%, interrupting antiepileptic medication administration 14.39%, watching too much TV 14.39%, physical fatigue 12.59%. The number of seizure triggers can be mathematically modelled according to age and treatment resistance. Unresponsiveness to treatment of the epilepsy has a few predictors: timing of the seizure occurrence, imaging alterations, late psychomotor development, IQ, the number of seizure triggering factors. Conclusions. There was at least one seizure trigger identified in 79.9% of children with epilepsy. The most frequent reported trigger was sleep deprivation. The number of seizure triggers can be estimated through mathematical modelling. Treatment resistance of epileptic seizures has more predicting factors.
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Vaišvilas, M., A. Jasionis, and R. Mameniškienė. "Epilepsija ir COVID-19: neurologo, paciento ir nacionalinės sveikatos sistemos iššūkiai pandemijos metu." Neurologijos seminarai 24, no. 84 (July 1, 2020): 112–18. http://dx.doi.org/10.29014/ns.2020.15.

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Nors dažniausiai COVID-19 pasireiškia respiracinio pobūdžio simptomais ir rečiau pasitaikančiu daugybiniu organų nepakankamumu, infekuotiems asmenims galimi ir įvairūs neurologiniai simptomai. Publikuoti COVID-19 sukeltų traukulių atvejai, nors jų sąsaja su epilepsija – abejotina. Sergančiam epilepsija asmeniui, užsikrėtus COVID-19 ir taikant gydymą priešvirusiniais vaistais, svarbi jų sąveika su vartojamais vaistais nuo epilepsijos. Psichologinė pacientų būsena taip pat yra svarbus veiksnys priepuolių kontrolei, o pandemija keičia lėtinėmis ligomis sergančiųjų priežiūrą. Šiame straipsnyje pateikiame literatūros apžvalgą apie simptominių traukulių, epilepsinės būklės gydymą, taip pat epilepsija sergančių asmenų priežiūrą COVID-19 pandemijos metu. Pateikiame naujausias rekomendacijas elektroencefalografijos tyrimo atlikimui.
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Echeverría Hernández, N., M. D. M. Lázaro Redondo, F. de la Torre Brasas, A. Duque Domínguez, A. Mas Villaseñor, C. García Montero, L. Martín Díaz, and M. Otalora Navarro. "Psychoses of epilepsy – “Acute attacks of insanity”. What literature says and how we act." European Psychiatry 33, S1 (March 2016): S630. http://dx.doi.org/10.1016/j.eurpsy.2016.01.2364.

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IntroductionPatients with epilepsy seem particularly liable to certain major psychiatric disorders. Prevalence of schizophrenia within an epileptic population varies between 3% and 7% (1% in general population). The aetiology is possibly multifactorial (drugs and neurosurgery).ObjectivesTo study comorbidity between psychoses and epilepsy and management in the literature and in our patients.AimsTo analyze factors that might influence the onset of psychoses within an epileptic population and how this potential association could influence our practice.MethodsPubMed search was conducted with interest in psychoses of epilepsy, pharmacology, and comorbidity. Up to 10 variables related with factors influencing psychotic episodes that required hospital admission in three patients with epilepsy were studied.ResultsUnlike published data, our patients did not have postictal psychoses. All cases had early onset temporal lobe epilepsy with no seizure activity since diagnosis (more than 20 years). No family history of either epilepsy or psychoses. Management included lamotrigine, oxcarbazepine, carbamazepine, zonisamide, and levetiracetam in conventional doses. The psychosis, which comprised affective, schizophrenic, and confusional elements, lasted longer and was more troublesome than psychosis in non-epileptic patients. Response to neuroleptics was poorer than in non-epileptic patients with psychoses. Consultation with Neurology Unit resulted in end of treatment with zonisamide and levetiracetam.ConclusionsLess than perfect evidence suggests the association between psychosis and epilepsy. In our patients, no postictal cases were recorded. Management showed poorer effect of neuroleptics when compared with non-epileptics, and zonisamide and levetiracetam were changed for other drugs with presumably lower association with psychoses.Disclosure of interestThe authors have not supplied their declaration of competing interest.
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Adoukonou, Thierry, Mendinatou Agbétou, Rachidi Imorou Sidi, Colombe Gnansounou, Donald Accrombessi, Yasmine Hounzangbe-Adoukonou, Dieudonné Gnonlonfoun, Salifou Kabibou, Josiane Angéline Tonato-Bagnan, and Dismand Houinato. "Prognosis of Pregnancy in Epileptics in Benin: A Case–Control Study." Journal of Neurosciences in Rural Practice 11, no. 03 (June 12, 2020): 395–402. http://dx.doi.org/10.1055/s-0040-1709366.

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Abstract Objective The main purpose of this article is to define prognosis of pregnancies in epileptic women in Benin. Methods This was a case–control study that included 54 epileptic women who had at least one pregnancy matched to 162 controls on age, pregnancy term, and monitoring center. Information about epilepsy, treatment, pregnancy, and childbirth were collected. A logistic regression with odds ratio (OR) calculation was used to study the association. Results During pregnancy 22.22% of epileptic women experienced an increase in seizure frequency. Epileptics had more frequent miscarriages (OR: 1.84 [1.01–3.51]), more incidents during pregnancy (OR: 4.03 [1.04–15.60]), and were more often hospitalized (OR: 3.35 [1.46–7.69]) than women without epilepsy. They, more often, had premature children before 37 weeks of amenorrhea (OR: 2.10 [1.12–3.91]) and gave birth to low-birth-weight children (OR = 2.17 [1.00–4.76]). Conclusion Occurrence of a pregnancy in an epileptic woman in Benin is at risk and requires multidisciplinary monitoring by both neurologist and obstetrician to reduce complications.
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Tosetti, Maria F. Valls, Miriam A. Campos, Claudia R. Bauer, Márcia M. Araujo, Sibelle Pedrazolli, Yara B. Silva, Cristina Montovani, et al. "Knowledge about epilepsy among teachers and epileptic patients." Arquivos de Neuro-Psiquiatria 49, no. 3 (September 1991): 255–59. http://dx.doi.org/10.1590/s0004-282x1991000300004.

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223 epileptics patients and their families and 136 teachers from public and private schools were submitted to similar questionnaires related to inheritance, transmission, cure, complilcation rates, care during seizures, need for information on the disease, habits, comparison with other diseases and to the educational and social performances of epileptics. Cure and complication nates accounted for the main differences between those populations. Epileptics could recognize a bigger number of complications but still expected to be cured from the disease. The majority of teachers and patients have never been informed about epilepsy and this finding was related to the big number of equivocal answers obtained from them. Put together, the data showed that social and educational performance of epileptic patients could be disturbed by medical and social parameters. Some, of them could be improved by an educational program towards these aspects of epilepsy.
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Kulshreshtha, Dinkar, Pradeep Maurya, Ajai Singh, and Anup Thacker. "Withdrawal of anti-epileptic drugs: A review." International Journal of Epilepsy 02, no. 01 (June 2015): 038–43. http://dx.doi.org/10.1016/j.ijep.2015.03.002.

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AbstractAnti-epileptic drugs are the mainstay in treatment of epilepsy. It requires a strong clinical decision in patients who are well controlled on medications to withdraw anti-epileptic drugs. This decision has to be based on the clinical profile, epilepsy type, neuroimaging and electroencephalography (EEG) findings and has to be more individualized as per the patient needs. In the context of drug withdrawal, it is necessary to look into the details of why, how and when to withdraw anti-epileptics. In this article, we critically try to answer such queries and look into the established guidelines with respect to drug withdrawal. We shall look into the chances of recurrence on stopping these drugs. Also, in the end we shall discuss briefly some special clinical scenarios where decision to stop anti-epileptic drugs is a challenging task.
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41

Khosravani, Houman, and Gerald W. Zamponi. "Voltage-Gated Calcium Channels and Idiopathic Generalized Epilepsies." Physiological Reviews 86, no. 3 (July 2006): 941–66. http://dx.doi.org/10.1152/physrev.00002.2006.

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The idiopathic generalized epilepsies encompass a class of epileptic seizure types that exhibit a polygenic and heritable etiology. Advances in molecular biology and genetics have implicated defects in certain types of voltage-gated calcium channels and their ancillary subunits as important players in this form of epilepsy. Both T-type and P/Q-type channels appear to mediate important contributions to seizure genesis, modulation of network activity, and genetic seizure susceptibility. Here, we provide a comprehensive overview of the roles of these channels and associated subunits in normal and pathological brain activity within the context of idiopathic generalized epilepsy.
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42

Ali, Irfan, and Dave F. Clarke. "Febrile Seizure Plus and PCDH19-Related Epilepsy Syndromes." Journal of Pediatric Epilepsy 08, no. 03 (September 2019): 074–78. http://dx.doi.org/10.1055/s-0040-1701202.

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AbstractEpilepsy is a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures. Practically, a patient has epilepsy if having two unprovoked seizures more than 24 hours apart, one unprovoked seizure and significant risk of another seizure, or epilepsy syndrome. Seizures induced by fever do not therefore fit this classification. An initial febrile seizure may therefore cause a false sense of security in children who evolve to febrile seizure plus syndromes. Sodium channel defects seem to predominate as the main causative factor for febrile seizure plus syndromes. More severe pathological variants, such as Dravet's syndrome, have phenotypic similarities to other fever-associated epileptic encephalopathies, including those caused by mutations in protocadherin 19 (PCDH19). The clinical presentations, investigational studies, and management of febrile seizure plus syndrome, as well as epilepsies associated with PCDH19 mutations will be reviewed.
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43

Szepetowski, Pierre. "Genetics Studies in Idiopathic Focal Epilepsies in Childhood." Journal of Pediatric Epilepsy 05, no. 03 (July 1, 2016): 139–41. http://dx.doi.org/10.1055/s-0036-1585065.

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Numerous “epilepsy genes” have been identified in the recent years, thanks to the recent progress in massive parallel sequencing and genome analysis. Among the formerly called “idiopathic” childhood focal epilepsies, a first and major gene responsible for focal epilepsies and epileptic encephalopathies with speech and language dysfunction (the epilepsy–aphasia spectrum, EAS), GRIN2A, has been identified. GRIN2A encodes the GluN2A subunit of N-methyl-D-aspartate receptors, which are gated by the excitatory neurotransmitter glutamate. More than 60 mutations of various types and with various functional consequences in vitro have been reported. Several rare genetic variants that may influence EAS have been reported in a few other genes. The identification of GRIN2A as a first cause of EAS represents a first key point that will help in deciphering the underlying pathophysiology and in understanding the clinical heterogeneity and variability seen in the patients and families.
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44

Guilhoto, Laura M. F. F. "Revisão terminológica e conceitual para organização de crises e epilepsias: relato da Comissão da ILAE de Classificação e Terminologia, 2005-2009. Novos Paradigmas?" Journal of Epilepsy and Clinical Neurophysiology 17, no. 3 (2011): 100–105. http://dx.doi.org/10.1590/s1676-26492011000300005.

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Introdução: A organização das crises epilépticas e epilepsias vem sendo descrita em classificações organizadas pela Liga Internacional contra a Epilepsia (International League Against Epilepsy, ILAE) há cerca de meio século. Segundo estes documentos iniciais aperfeiçoados na década de 1980, as crises foram divididas em focais ou generalizadas, de acordo com o seu modo de início, ou em uma região específica do cérebro ou de forma bilateral, respectivamente. A etiologia das epilepsias foi considerada idiopática, sintomática ou criptogênica. Recentemente ampla discussão na comunidade científica surgiu após a publicação em 2010 de uma revisão terminológica e conceitual da Comissão de Classificação e Terminologia da ILAE. Objetivo/Método: Divulgação em Português do resumo e comentários da discussão da “Revisão terminológica e conceitual para organização de crises e epilepsias: Relato da Comissão de Classificação e Terminologia da ILAE, 2005-2009” a fim de apresentá-la aos profissionais da área de saúde dos países de língua portuguesa. Resultados: Os termos generalizado e focal foram redefinidos; crises que ocorrem em redes neuronais bilateralmente distribuídas que rapidamente as engajam são generalizadas; e aquelas que ocorrem dentro de redes delimitadas a um hemisfério ou discretamente localizadas ou mais amplamente distribuídas são focais. A classificação de crises generalizadas foi simplificada. As crises focais devem ser descritas de acordo com suas manifestações (por ex., discognitiva, motora, etc). Os conceitos generalizado e focal não se aplicam a síndromes eletroclínicas. Genético, metabólico-estrutural e desconhecido representam conceitos modificados para substituir os termos idiopático, simtomático e criptogênico, respectivamente. Nem todas as epilepsias são reconhecidas como síndromes eletroclínicas. A organização da epilepsia é feita pela especificadade, a saber, síndromes eletroclínicas, epilepsias não sindrômicas com causa estrutural ou metabólica, e epilepsias de causa desconhecida. Classes naturais (por ex. causa específica subjacente, idade de início, tipos associados de crises) ou agrupamentos pragmáticos (por ex. encefalopatia epiléptica, síndromes eletroclínicas auto-limitadas) podem servir tanto para organizar o conhecimento sobre formas reconhecidas de epilepsia como facilitar a identificação de outras novas. Várias opiniões dos especialistas internacionais sobre essa terminologia foram divulgadas e uma revisão ampliada será apresentada em 2013 pela Comissão de Classificação e Terminologia da ILAE. Conclusão: A Comissão de Classificação e Terminologia da ILAE (2005-2009) revisou conceitos, terminologia e abordagens para classificar crises e formas de epilepsia tendo publicado em 2010 os resultados do grupo de discussão vigentes nessa data e os resultados finais serão divulgados em 2013.
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45

TREVISOL-BITTENCOURT, PAULO CÉSAR, VICTOR REIS DA SILVA, MÁRCIO ALCIDES MOLINARI, and ANDRÉ RIBEIRO TROIANO. "Phenytoin as the first option in female epileptic patients?" Arquivos de Neuro-Psiquiatria 57, no. 3B (September 1999): 784–86. http://dx.doi.org/10.1590/s0004-282x1999000500008.

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OBJECTIVE: Phenytoin (PHT) is one of the first-choice drugs in several epileptic syndromes, mostly in partial epilepsies, in which case it is effective as carbamazepine and phenobarbital. However, like any other anti-epileptic drug (AED), unpleasant side-effects are not rare. The aim of this study is the evaluation of dermatological troubles related to chronic PHT usage in female patients. METHOD: Between 1990-93, 731 new patients underwent investigation for epilepsy at the Multidisciplinary Clinic for Epilepsy in our State. In this sample 283 were AED users at the time of the first assessment. Sixty one female patients taking PHT were identified. They were taking PHT in a dosage ranging from 100 to 300 mg daily, in mono or polytherapy regimen, during 1-5 previous years. RESULTS: More than 50% of the sample showed coarse facial features made by the combination of several degrees of acne, hirsutism and gingival hyperplasia. CONCLUSION: Except in emergency situations, PHT should not be prescribed as the first option to the treatment of female epileptic patients, because not uncommonly the cosmetic side-effects are more socially handicapping than the epileptic syndrome by itself.
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46

Sills, Graeme J. "Seizures Beget Seizures: A Lack of Experimental Evidence and Clinical Relevance Fails to Dampen Enthusiasm." Epilepsy Currents 7, no. 4 (July 2007): 103–4. http://dx.doi.org/10.1111/j.1535-7511.2007.00189.x.

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Three Brief Epileptic Seizures Reduce Inhibitory Synaptic Currents, GABAACurrents, and GABAA-Receptor Subunits. Evans MS, Cady CJ, Disney KE, Yang L, LaGuardia JJ. Epilepsia 2006;4710):1655–1664. PURPOSE: Cellular mechanisms activated during seizures may exacerbate epilepsy. γ-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in brain, and we hypothesized that brief epileptic seizures may reduce GABA function. METHODS: We used audiogenic seizures (AGSs) in genetically epilepsy-prone rats (GEPRs) to investigate effects of seizures on GABA-mediated inhibition in the presence of epilepsy. GEPRs are uniformly susceptible to AGSs beginning at 21 postnatal days. AGSs are brief convulsions lasting 20 s, and they begin in inferior colliculus (IC). We evoked three seizures in GEPRs and compared the results with those in seizure-naive GEPRs and nonepileptic Sprague-Dawley (SD) rats, the GEPR parent strain. RESULTS: Whole-cell recording in IC slices showed that GABA-mediated monosynaptic inhibitory postsynaptic currents (IPSCs) were reduced 55% by three brief epileptic seizures. Whole-cell recording in IC neuronal cultures showed that currents elicited by GABA were reduced 67% by three seizures. Western blotting for the alpha1 and alpha4 subunits of the GABAA receptor showed no statistically significant effects. In contrast, three brief epileptic seizures reduced gamma2 subunit levels by 80%. CONCLUSIONS: The effects of the very first seizures, in animals known to be epileptic, in an area of brain known to be critical to the seizure network, were studied. The results indicate that even brief epileptic seizures can markedly reduce IPSCs and GABA currents and alter GABAA-receptor subunit protein levels. The cause of the reductions in IPSCs and GABA currents is likely to be altered receptor subunit composition, with reduced gamma2 levels causing reduced GABAA-receptor sensitivity to GABA. Seizure-induced reductions in GABA-mediated inhibition could exacerbate epilepsy.
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47

Sanya, E. O., T. A. T. Salami, O. O. Goodman, O. I. N. Buhari, and M. O. Araoye. "Perception and attitude to epilepsy among teachers in primary, secondary and tertiary educational institutions in middle belt Nigeria." Tropical Doctor 35, no. 3 (July 1, 2005): 153–56. http://dx.doi.org/10.1258/0049475054620905.

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Compared with the disability associated with repeated seizures or side-effects of antiepileptic medications, the social stigma associated with epilepsy is often a major handicap to people living with this condition. This study therefore looked at the knowledge, attitude and perception of teachers who see a lot of epileptics, relates on daily bases and have a high influence on students with epilepsy. Self-administered questionnaires were used to obtain information from 460 randomly selected teachers in primary, secondary and tertiary educational institutions in Kwara State-middle belt of Nigeria. The response rate was 75%. Almost all of the teachers had heard about epilepsy, but their awareness does not equate with the acceptance and understanding of epilepsy. About 30.5% believed that it could be contracted through the saliva of an epileptic, 27.7% thought it was synonymous with possession with evil spirit, while 10% misunderstood epilepsy for insanity. Close to one-fifth of the teachers were of the opinion that epileptic students have a below average mental capacity compared with other students and so cannot attainment the highest possible education. Negative attitude and bias towards epilepsy is still deeply ingrained among teachers in Nigeria. Apart from formal education, teachers need to have health education courses on common disease conditions such as epilepsy that are prevalent in school age. This might help to reduce prejudice and increase the acceptance of epileptic individuals into the classroom.
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48

Blume, Warren T. "Future Directions in Pediatric Epileptology." Journal of Child Neurology 9, no. 2_suppl (October 1994): 2S74–2S78. http://dx.doi.org/10.1177/0883073894009002111.

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Rapid developments in several areas of epileptology alter or clarify concepts and bring new hope to epileptic patients and their associates. Brief discussions of such advances comprise this report. Experimental and clinical data concerning the pathogenesis of cognitive impairment in some epileptic conditions are reviewed. Epidemiologic studies have altered some long-held concepts concerning etiology of seizures in early life. Molecular genetic studies have disclosed abnormalities in some of the epilepsies: a genetic predisposition to epilepsy may explain why some patients with cortical lesions develop seizures and others do not. It is suggested that many questions regarding surgery in pediatric epilepsy will be resolved only by more reliable techniques of case selection and follow-up. Practitioners in developed countries must realize how rudimentary is the care given to the unfortunate many with seizure disorders in less advantaged areas. (J Child Neurol 1994;9(Suppl)2S74-2S78).
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49

José Antonio García Martínez, Maria Candelaria Benimeli López, Francisco García-Legaz Navarro, and Carlos García Palenciano. "Estatus epiléptico refractario no convulsionante en postoperatorio de pancreatectomía total: A propósito de un caso." Revista Electrónica AnestesiaR 10, no. 12 (January 2, 2019): 2. http://dx.doi.org/10.30445/rear.v10i12.653.

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Se presenta un caso clinico de Estatus Epileptico No convulsionante en el posopoeratorio de una paciente de 79 años sin antecedentes de epilepsia, y su probable relación con la antibioterapia pautada. Seguidamente se realiza una discusion acerca del estatus epileptico y su aparicion como efecto secundario del tratamiento con ciertos antibioticos. ABSTRACT We present a clinical case of non-convulsive epileptic status in the post-operative of a 79-year-old patient with no history of epilepsy, and its probable relationship with scheduled antibiotic therapy. Then a discussion about the epileptic status and its appearance as a side effect of the treatment with certain antibiotics is made.
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50

Edwards, Jonathan C. "Seizure Types, Epilepsy Syndromes, Etiology, and Diagnosis." CNS Spectrums 6, no. 9 (September 2001): 750–55. http://dx.doi.org/10.1017/s1092852900001498.

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ABSTRACTThe clinical manifestation of epileptic seizures may vary widely from patient to patient, depending on the region of the brain involved. Over the centuries, many seizure classific systems have been used, and the current most widely used classification system is that of the International League Against Epilepsy (ILAE). The ILAE system divides seizures into those of partial onset and those of generalized onset, depending on whether the initial clinical manifestations indicate that one cortical region or both hemispheres are involved at the onset of the seizure. Partial seizures are then divided into simple partial seizures, in which a fully conscious state is retained, or complex partial seizures, in which consciousness is impaired. A more recent classification system based purely on symptom features and signs has been proposed, and this system may provide advantages for localization, and especially for surgical evaluation. Epilepsy is a condition characterized by recurrent unprovoked seizures. Epilepsy may be idiopathic, cryptogenic, or symptomatic. Idiopathic epilepsies are generally genetic, and while man such syndromes have been described, advances in molecular genetics will undoubtedly reveal many more syndromes in near future. Cryptogenic epilepsies are those in which an underlying cause is suspected, but the etiology remains undetected. Epilepsies for which there is an underlying structural cause or major metabolic derangement are considered symptomatic. Common causes and diagnostic evaluation are described in this article.
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