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Littérature scientifique sur le sujet « Nocturnal Frontal Lobe Epilepsy »

Auteur : Grafiati
Publié le 9 mars 2023
Mis à jour le 10 mars 2023

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Articles de revues sur le sujet "Nocturnal Frontal Lobe Epilepsy"

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Millichap, J. Gordon. « Nocturnal Frontal Lobe Epilepsy ». Pediatric Neurology Briefs 13, no 6 (1 juin 1999) : 47. http://dx.doi.org/10.15844/pedneurbriefs-13-6-10.

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Millichap, J. Gordon. « Nocturnal Frontal Lobe Epilepsy ». Pediatric Neurology Briefs 10, no 10 (1 octobre 1996) : 74. http://dx.doi.org/10.15844/pedneurbriefs-10-10-2.

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Ferini-Strambi, L. « Nocturnal frontal lobe epilepsy ». Electroencephalography and Clinical Neurophysiology 103, no 1 (juillet 1997) : 61. http://dx.doi.org/10.1016/s0013-4694(97)88179-9.

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Ryvlin, Philippe, Sylvain Rheims et Gail Risse. « Nocturnal Frontal Lobe Epilepsy ». Epilepsia 47, s2 (novembre 2006) : 83–86. http://dx.doi.org/10.1111/j.1528-1167.2006.00698.x.

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Millichap, J. Gordon. « Nocturnal Familial Frontal Lobe Epilepsy ». Pediatric Neurology Briefs 12, no 3 (1 mars 1998) : 18. http://dx.doi.org/10.15844/pedneurbriefs-12-3-2.

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Oldani, Alessandro, Luigi Ferini-Strambi et Marco Zucconi. « Symptomatic nocturnal frontal lobe epilepsy ». Seizure 7, no 4 (août 1998) : 341–43. http://dx.doi.org/10.1016/s1059-1311(98)80030-7.

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Scheffer, Ingrid E., Kailash P. Bhatia, Iscia Lopes-Cendes, David R. Fish, C. David Marsden, Eva Andermann, Frederick Andermann et al. « Autosomal dominant nocturnal frontal lobe epilepsy ». Brain 118, no 1 (février 1995) : 61–73. http://dx.doi.org/10.1093/brain/118.1.61.

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Scheffer, Ingrid E. « Autosomal Dominant Nocturnal Frontal Lobe Epilepsy ». Epilepsia 41, no 8 (août 2000) : 1059–60. http://dx.doi.org/10.1111/j.1528-1157.2000.tb00298.x.

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Derry, Christopher. « Nocturnal Frontal Lobe Epilepsy vs Parasomnias ». Current Treatment Options in Neurology 14, no 5 (5 août 2012) : 451–63. http://dx.doi.org/10.1007/s11940-012-0191-8.

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Bonanni, Paolo, Anna Volzone, Giovanna Randazzo, Lisa Antoniazzi, Angelica Rampazzo, Maurizio Scarpa et Lino Nobili. « Nocturnal frontal lobe epilepsy in mucopolysaccharidosis ». Brain and Development 36, no 9 (octobre 2014) : 826–29. http://dx.doi.org/10.1016/j.braindev.2013.12.002.

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Thèses sur le sujet "Nocturnal Frontal Lobe Epilepsy"

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SANSONI, VERONICA. « Nocturnal frontal lobe epilepsy and febrile seizures : genetic and molecular aspects ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/41877.

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Idiopathic epilepsies are common and devastating neurological disorders in which genetic background and physiopathological mechanisms underlying the clinical phenotype are not fully characterized yet. These diseases are assumed to have a strong genetic component, being monogenic or oligo/polygenic with different recurrence risks in the same family. However, even in monogenic epilepsy, additional genes and environmental factors may modulate its expression, thus resulting in incomplete penetrance and variable phenotype. Ethiology, phenotypic manifestations and prognosis are indeed highly heterogeneous. Idiopathic epilepsies represent about 30-40% of all epilepsies in childhood and 20% in adults. Most of them are complex diseases: patients may shift from one phenotype to another during their lifetime and parents affected by one form may have children suffering from another epileptic syndrome. The identification of genes responsible for distinct epilepsy syndromes or influencing the risk for epilepsy has important implications, for both research and clinical purposes. In this work we studied the genetic bases of two different epilepsies: nocturnal frontal lobe epilepsy (NFLE/ADNFLE) and febrile seizures (FS/GEFS+). In the case of the NFLE/ADNFLE phenotype, we performed a mutational screening of known genes, including CRH and its promoter, in a sample of both sporadic and familial patients. The study allowed the identification of: an already known mutation in the CHRNA4 gene (p.Ser284Leu) originated de novo in one NFLE patient; three unknown variants in the CRH promoter in both sporadic and familial patients which we demonstrated to not cosegregate with the disease; one unknown missense mutation in the coding portion of the CRH gene in one ADNFLE patient. By functional in vitro analysis we demonstrated that the missense mutation causes impairment in the production and release of the CRH hormone. This impairment could be related to an altered capability of patients to respond quickly to stress agents. Finally, by analyzing candidate genes encoding the orexin system we demonstrated an unlikely role of this system in the pathogenesis of ADNFLE: none of the patients has mutations in the three genes. In the study of FS/GEFS+ phenotype, the role of the SCN1A gene was evaluated. Several intronic and exonic polymorphisms were detected. In the case of unknown intronic variants, an in silico analysis revealed that these variations do not introduce or remove any splicing sites. Interestingly, we found in a patient two missense mutations. These two variants co-segregated with the pathology being present in all affected individuals and in two obligate carriers. Owing to the location of both mutations in important regions of the sodium channel, we are now testing the hypothesis of their causative role in the pathogenesis of this family’s disease. The study will allow the evaluation of the effect of these mutations (considered either singly or in conjunction with the other) on the activation/inactivation properties of the sodium channel in the presence/absence of the β-1 accessory subunit.
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Calandra, Buonaura Giovanna <1973&gt. « Wavelet analysis of heart rate variability related to nocturnal frontal lobe epilepsy seizures ». Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2782/1/Calandra_Giovanna_tesi.pdf.

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Introduction: Nocturnal frontal lobe epilepsy (NFLE) is a distinct syndrome of partial epilepsy whose clinical features comprise a spectrum of paroxysmal motor manifestations of variable duration and complexity, arising from sleep. Cardiovascular changes during NFLE seizures have previously been observed, however the extent of these modifications and their relationship with seizure onset has not been analyzed in detail. Objective: Aim of present study is to evaluate NFLE seizure related changes in heart rate (HR) and in sympathetic/parasympathetic balance through wavelet analysis of HR variability (HRV). Methods: We evaluated the whole night digitally recorded video-polysomnography (VPSG) of 9 patients diagnosed with NFLE with no history of cardiac disorders and normal cardiac examinations. Events with features of NFLE seizures were selected independently by three examiners and included in the study only if a consensus was reached. Heart rate was evaluated by measuring the interval between two consecutive R-waves of QRS complexes (RRi). RRi series were digitally calculated for a period of 20 minutes, including the seizures and resampled at 10 Hz using cubic spline interpolation. A multiresolution analysis was performed (Daubechies-16 form), and the squared level specific amplitude coefficients were summed across appropriate decomposition levels in order to compute total band powers in bands of interest (LF: 0.039062 - 0.156248, HF: 0.156248 - 0.624992). A general linear model was then applied to estimate changes in RRi, LF and HF powers during three different period (Basal) (30 sec, at least 30 sec before seizure onset, during which no movements occurred and autonomic conditions resulted stationary); pre-seizure period (preSP) (10 sec preceding seizure onset) and seizure period (SP) corresponding to the clinical manifestations. For one of the patients (patient 9) three seizures associated with ictal asystole were recorded, hence he was treated separately. Results: Group analysis performed on 8 patients (41 seizures) showed that RRi remained unchanged during the preSP, while a significant tachycardia was observed in the SP. A significant increase in the LF component was instead observed during both the preSP and the SP (p<0.001) while HF component decreased only in the SP (p<0.001). For patient 9 during the preSP and in the first part of SP a significant tachycardia was observed associated with an increased sympathetic activity (increased LF absolute values and LF%). In the second part of the SP a progressive decrease in HR that gradually exceeded basal values occurred before IA. Bradycardia was associated with an increase in parasympathetic activity (increased HF absolute values and HF%) contrasted by a further increase in LF until the occurrence of IA. Conclusions: These data suggest that changes in autonomic balance toward a sympathetic prevalence always preceded clinical seizure onset in NFLE, even when HR changes were not yet evident, confirming that wavelet analysis is a sensitive technique to detect sudden variations of autonomic balance occurring during transient phenomena. Finally we demonstrated that epileptic asystole is associated with a parasympathetic hypertonus counteracted by a marked sympathetic activation.
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Calandra, Buonaura Giovanna <1973&gt. « Wavelet analysis of heart rate variability related to nocturnal frontal lobe epilepsy seizures ». Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2782/.

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Introduction: Nocturnal frontal lobe epilepsy (NFLE) is a distinct syndrome of partial epilepsy whose clinical features comprise a spectrum of paroxysmal motor manifestations of variable duration and complexity, arising from sleep. Cardiovascular changes during NFLE seizures have previously been observed, however the extent of these modifications and their relationship with seizure onset has not been analyzed in detail. Objective: Aim of present study is to evaluate NFLE seizure related changes in heart rate (HR) and in sympathetic/parasympathetic balance through wavelet analysis of HR variability (HRV). Methods: We evaluated the whole night digitally recorded video-polysomnography (VPSG) of 9 patients diagnosed with NFLE with no history of cardiac disorders and normal cardiac examinations. Events with features of NFLE seizures were selected independently by three examiners and included in the study only if a consensus was reached. Heart rate was evaluated by measuring the interval between two consecutive R-waves of QRS complexes (RRi). RRi series were digitally calculated for a period of 20 minutes, including the seizures and resampled at 10 Hz using cubic spline interpolation. A multiresolution analysis was performed (Daubechies-16 form), and the squared level specific amplitude coefficients were summed across appropriate decomposition levels in order to compute total band powers in bands of interest (LF: 0.039062 - 0.156248, HF: 0.156248 - 0.624992). A general linear model was then applied to estimate changes in RRi, LF and HF powers during three different period (Basal) (30 sec, at least 30 sec before seizure onset, during which no movements occurred and autonomic conditions resulted stationary); pre-seizure period (preSP) (10 sec preceding seizure onset) and seizure period (SP) corresponding to the clinical manifestations. For one of the patients (patient 9) three seizures associated with ictal asystole were recorded, hence he was treated separately. Results: Group analysis performed on 8 patients (41 seizures) showed that RRi remained unchanged during the preSP, while a significant tachycardia was observed in the SP. A significant increase in the LF component was instead observed during both the preSP and the SP (p<0.001) while HF component decreased only in the SP (p<0.001). For patient 9 during the preSP and in the first part of SP a significant tachycardia was observed associated with an increased sympathetic activity (increased LF absolute values and LF%). In the second part of the SP a progressive decrease in HR that gradually exceeded basal values occurred before IA. Bradycardia was associated with an increase in parasympathetic activity (increased HF absolute values and HF%) contrasted by a further increase in LF until the occurrence of IA. Conclusions: These data suggest that changes in autonomic balance toward a sympathetic prevalence always preceded clinical seizure onset in NFLE, even when HR changes were not yet evident, confirming that wavelet analysis is a sensitive technique to detect sudden variations of autonomic balance occurring during transient phenomena. Finally we demonstrated that epileptic asystole is associated with a parasympathetic hypertonus counteracted by a marked sympathetic activation.
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Puligheddu, Monica Maria Francesca <1969&gt. « Rationale for an adjunctive therapy with fenofibrate in pharmacoresistant nocturnal frontal lobe epilepsy (NFLE) ». Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/7057/1/M_Puligheddu_TESI_Dottorato.pdf.

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Nocturnal Frontal Lobe Epilepsy (NFLE) is characterized by onset during infancy or childhood with persistence in adulthood, family history of similar nocturnal episodes simulating non-REM parasomnias (sleep terrors or sleepwalking), general absence of morphological substrates, often by normal interictal electroencephalographical recordings (EEGs) during wakefulness. A family history of epilepsy may be present with Mendelian autosomal dominant inheritance has been described in some families. Recent studies indicate the involvement of neuronal nicotinic acetylcholine receptors (nAChRs) in the molecular mechanisms of NFLE. Mutations in the genes encoding for the α4 (CHRNA4) and ß2 (CHRNB2) subunits of the nAChR induce changes in the biophysical properties of nAChR, resulting generally in a “gain of function”. Preclinical studies report that activation of a nuclear receptor called type peroxisome proliferator-activated receptor (PPAR-α) by endogenous molecules or by medications (e.g. fenofibrate) reduces the activity of the nAChR and, therefore, may decrease the frequency of seizures. Thus, we hypothesize that negative modulation of nAChRs might represent a therapeutic strategy to be explored for pharmacological treatment of this form of epilepsy, which only partially responds to conventional antiepileptic drugs. In fact, carbamazepine, the current medication for NFLE, abolishes the seizures only in one third of the patients. The aim of the project is: 1)_to verify the clinical efficacy of adjunctive therapy with fenofibrate in pharmacoresistant NFLE and ADNFLE patients; focousing on the analysis of the polysomnographic action of the PPAR- agonist (fenofibrate). 2)_to demonstrate the subtended mechanism of efficacy by means of electrophysiological and behavioral experiments in an animal model of the disease: particularly, transgenic mice carrying the mutation in the nAChR 4 subunit (Chrna4S252F) homologous to that found in the humans. Given that a PPAR-α agonist, FENOFIBRATE, already clinically utilized for lipid metabolism disorders, provides a promising therapeutic avenue in the treatment of NFLE\ADNFLE.
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Puligheddu, Monica Maria Francesca <1969&gt. « Rationale for an adjunctive therapy with fenofibrate in pharmacoresistant nocturnal frontal lobe epilepsy (NFLE) ». Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/7057/.

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Nocturnal Frontal Lobe Epilepsy (NFLE) is characterized by onset during infancy or childhood with persistence in adulthood, family history of similar nocturnal episodes simulating non-REM parasomnias (sleep terrors or sleepwalking), general absence of morphological substrates, often by normal interictal electroencephalographical recordings (EEGs) during wakefulness. A family history of epilepsy may be present with Mendelian autosomal dominant inheritance has been described in some families. Recent studies indicate the involvement of neuronal nicotinic acetylcholine receptors (nAChRs) in the molecular mechanisms of NFLE. Mutations in the genes encoding for the α4 (CHRNA4) and ß2 (CHRNB2) subunits of the nAChR induce changes in the biophysical properties of nAChR, resulting generally in a “gain of function”. Preclinical studies report that activation of a nuclear receptor called type peroxisome proliferator-activated receptor (PPAR-α) by endogenous molecules or by medications (e.g. fenofibrate) reduces the activity of the nAChR and, therefore, may decrease the frequency of seizures. Thus, we hypothesize that negative modulation of nAChRs might represent a therapeutic strategy to be explored for pharmacological treatment of this form of epilepsy, which only partially responds to conventional antiepileptic drugs. In fact, carbamazepine, the current medication for NFLE, abolishes the seizures only in one third of the patients. The aim of the project is: 1)_to verify the clinical efficacy of adjunctive therapy with fenofibrate in pharmacoresistant NFLE and ADNFLE patients; focousing on the analysis of the polysomnographic action of the PPAR- agonist (fenofibrate). 2)_to demonstrate the subtended mechanism of efficacy by means of electrophysiological and behavioral experiments in an animal model of the disease: particularly, transgenic mice carrying the mutation in the nAChR 4 subunit (Chrna4S252F) homologous to that found in the humans. Given that a PPAR-α agonist, FENOFIBRATE, already clinically utilized for lipid metabolism disorders, provides a promising therapeutic avenue in the treatment of NFLE\ADNFLE.
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Rossi, Magi Lorenzo. « Graph-based analysis of brain resting-state fMRI data in nocturnal frontal lobe epileptic patients ». Master's thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amslaurea.unibo.it/8332/.

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Il lavoro che ho sviluppato presso l'unità di RM funzionale del Policlinico S.Orsola-Malpighi, DIBINEM, è incentrato sull'analisi dati di resting state - functional Magnetic Resonance Imaging (rs-fMRI) mediante l'utilizzo della graph theory, con lo scopo di valutare eventuali differenze in termini di connettività cerebrale funzionale tra un campione di pazienti affetti da Nocturnal Frontal Lobe Epilepsy (NFLE) ed uno di controlli sani. L'epilessia frontale notturna è una peculiare forma di epilessia caratterizzata da crisi che si verificano quasi esclusivamente durante il sonno notturno. Queste sono contraddistinte da comportamenti motori, prevalentemente distonici, spesso complessi, e talora a semiologia bizzarra. L'fMRI è una metodica di neuroimaging avanzata che permette di misurare indirettamente l'attività neuronale. Tutti i soggetti sono stati studiati in condizioni di resting-state, ossia di veglia rilassata. In particolare mi sono occupato di analizzare i dati fMRI con un approccio innovativo in campo clinico-neurologico, rappresentato dalla graph theory. I grafi sono definiti come strutture matematiche costituite da nodi e links, che trovano applicazione in molti campi di studio per la modellizzazione di strutture di diverso tipo. La costruzione di un grafo cerebrale per ogni partecipante allo studio ha rappresentato la parte centrale di questo lavoro. L'obiettivo è stato quello di definire le connessioni funzionali tra le diverse aree del cervello mediante l'utilizzo di un network. Il processo di modellizzazione ha permesso di valutare i grafi neurali mediante il calcolo di parametri topologici che ne caratterizzano struttura ed organizzazione. Le misure calcolate in questa analisi preliminare non hanno evidenziato differenze nelle proprietà globali tra i grafi dei pazienti e quelli dei controlli. Alterazioni locali sono state invece riscontrate nei pazienti, rispetto ai controlli, in aree della sostanza grigia profonda, del sistema limbico e delle regioni frontali, le quali rientrano tra quelle ipotizzate essere coinvolte nella fisiopatologia di questa peculiare forma di epilessia.
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Manfredi, I. « In vivo study of mutant nicotinic receptor's role in the pathogenesis of autosomal dominant nocturnal frontal lobe epilepsy : development and characterization of a conditional mouse model ». Doctoral thesis, Università degli Studi di Milano, 2008. http://hdl.handle.net/2434/63073.

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Upton, Dominic Richard Barrie. « Neuropsychological aspects of frontal lobe epilepsy ». Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309291.

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Derry, C. P. « Frontal lobe epilepsy, sleep and parasomnias ». Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445467/.

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A close relationship exists between sleep and epilepsy. While many forms of epilepsy may be influenced by the sleep-wake cycle, this phenomenon is particularly evident in frontal lobe epilepsy where affected individuals may experience seizures exclusively during sleep (nocturnal frontal lobe epilepsy, NFLE). In this thesis, three aspects of the relationship between sleep and frontal lobe epilepsy are examined. Firstly, serotonergic neurotransmission across the human sleep-wake cycle was studied using the novel PET ligand l8F-MPPF, a serotonergic 5HT)A receptor radioligand sensitive to endogenous serotonin release. Fourteen individuals with narcolepsy underwent 18F-MPPF PET scans during sleep and wakefulness. The study demonstrated a 13% increase in 18F-MPPF binding potential (p < 0.01) during sleep, indicating a reduction in serotoninergic neurotransmission, in line with existing animal data. Secondly, the characterisation of benign, non-epileptic parasomnias and their distinction from nocturnal frontal lobe seizures was addressed in two studies. The first comprised an analysis of the historical features of these conditions, and included the development and validation of a clinical scale for the diagnosis of nocturnal events. The second comprised a detailed semiological analysis of a series of parasomnias recorded on video-EEG monitoring, and a statistical comparison with seizures in NFLE. Although similarities between NFLE and parasomnias were observed, the results provide an evidence base for the confident distinction of these disorders. Finally, the familial form of NFLE (autosomal dominant nocturnal frontal lobe epilepsy, ADNFLE) is associated with mutations in genes for nicotinic acetylcholine receptor subunits, but recognised mutations account for only a minority of reported cases. The last study presented here is a clinical and genetic analysis of two large families with an unusually severe ADNFLE phenotype. Affected individuals had refractory epilepsy and increased rates of mental retardation and psychiatric disorders and, in one family, linkage studies suggest a previously unrecognised underlying mechanism.
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Petty, Karen Hammack. « Pediatric temporal lobe epilepsy versus frontal lobe epilepsy : how does cognitive performance differ ? / ». Full text available from ProQuest UM Digital Dissertations, 2007. http://0-proquest.umi.com.umiss.lib.olemiss.edu/pqdweb?index=0&did=1414130851&SrchMode=1&sid=2&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1221160824&clientId=22256.

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Livres sur le sujet "Nocturnal Frontal Lobe Epilepsy"

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Hans, Lüders, dir. Supplementary sensorimotor area. Philadelphia : Lippincott-Raven, 1996.

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Nobili, Lino, Paola Proserpio, Steve Gibbs et Giuseppe Plazzi. Sleep and epilepsy. Sous la direction de Sudhansu Chokroverty, Luigi Ferini-Strambi et Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0028.

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This chapter on sleep and epilepsy examines the activating and deactivating properties of NREM and REM sleep states on interictal epileptic activity and seizures. It reviews specific epileptic syndromes in which seizures manifest a tendency to present exclusively or predominantly during sleep or upon wakening. Particular attention is paid to the description of the different forms of nocturnal frontal lobe epilepsy: autosomal dominant and lesional. There is also a discussion of the negative bidirectional relationship between epilepsy and sleep disorders (sleep apneas and parasomnias) and the effect of pharmacological and nonpharmacological treatments. Finally, a brief review of the relationship between sleep and sudden unexpected death in epilepsy is given.
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Patrick, Chauvel, dir. Frontal lobe seizures and epilepsies. New York : Raven Press, 1992.

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(Editor), Patricia S. Goldman-Rakic, dir. Epilepsy and the Functional Anatomy of the Frontal Lobe (Advances in Neurology). Lippincott Williams & Wilkins, 1995.

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Wehner, Tim, Kanjana Unnwongse et Beate Diehl. Focal epilepsy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0028.

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This chapter examines the neurophysiology of focal epilepsy. It discusses the principles of EEG source localization. This is followed by a presentation of nonspecific and epileptiform interictal EEG findings and ictal EEG patterns seen in focal epilepsy, along with normal EEG variants that may be mistaken for epileptiform features. Seizure semiologies and ictal and interictal EEG findings in mesial and neocortical temporal lobe epilepsy, orbitofrontal, dorsolateral, and mesial frontal epilepsy, insular epilepsy, and parietal and occipital epilepsy are presented with illustrative case discussions derived from patients investigated for resective epilepsy surgery. A brief discussion of prognosis and treatment strategies for focal epilepsy follows.
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Elwes, Robert. Presurgical evaluation for epilepsy surgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0031.

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This chapter describes the preoperative electroclinical assessment of the various epilepsy syndromes and pathologies that are open to surgical treatment. Particular emphasis is placed on medial temporal epilepsy and frontal epilepsy. The assessment of cases considered for hemispherotomy, multiple subpial transection for Landau–Kleffner syndrome, anterior two-thirds callosotomy in symptomatic generalized epilepsy, neural stimulation, and cases with nodular hetertopia are summarized. Throughout the chapter, particular emphasis is placed on the need for multidisciplinary assessment, and the interpretation of the electroencephalogram (EEG) in the context of the clinical features, imaging, and neuropsychology. Evaluation pathways are suggested and the indications for intracranial EEG, the types of electrodes used and the operative complications are discussed in detail. Summaries of the key points in the electroclinical evaluation of temporal and frontal lobe epilepsy are given.
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Chapitres de livres sur le sujet "Nocturnal Frontal Lobe Epilepsy"

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Tinuper, Paolo, et Francesca Bisulli. « Autosomal Dominant Nocturnal Frontal Lobe Epilepsy ». Dans Atlas of Epilepsies, 1125–34. London : Springer London, 2010. http://dx.doi.org/10.1007/978-1-84882-128-6_166.

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Tinuper, P., G. Plazzi, F. Provini, A. Cerullo et E. Lugaresi. « The Syndrome of Nocturnal Frontal Lobe Epilepsy ». Dans Somatic and Autonomic Regulation in Sleep, 125–35. Milano : Springer Milan, 1997. http://dx.doi.org/10.1007/978-88-470-2275-1_8.

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Wong-Kisiel, Lily C., et Gregory A. Worrell. « Frontal Lobe Epilepsy ». Dans Epilepsy Case Studies, 139–44. Cham : Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-59078-9_25.

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Wong-Kisiel, Lily. « Frontal Lobe Epilepsy ». Dans Epilepsy Case Studies, 99–102. Cham : Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01366-4_22.

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Stern, John M., et Noriko Salamon. « Frontal Lobe Trauma ». Dans Imaging of Epilepsy, 125–27. Cham : Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-86672-3_30.

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Girvin, John P. « Frontal Lobe Surgery ». Dans Operative Techniques in Epilepsy, 165–200. Cham : Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-10921-3_7.

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Saint-Hilaire, Jean-Marc, Normand Giard, Guy Bouvier et Raymonde Labrecque. « Anterior Callosotomy in Frontal Lobe Epilepsies ». Dans Epilepsy and the Corpus Callosum, 303–14. Boston, MA : Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2419-5_14.

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Giard, N., I. Rouleau, A. Bouthillier, G. Bouvier et J. M. Saint-Hilaire. « Anterior Callosotomy Added to Frontal Lobectomy in Frontal Lobe Epilepsy ». Dans Epilepsy and the Corpus Callosum 2, 191–200. Boston, MA : Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-1427-9_18.

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Hernandez, Maria Teresa, Hannelore C. Sauerwein, Elaine de Guise, Anne Lortie, Isabelle Jambaqué, Olivier Dulac et Maryse Lassonde. « Neuropsychology of Frontal Lobe Epilepsy in Children ». Dans Advances in Behavioral Biology, 103–11. Boston, MA : Springer US, 2001. http://dx.doi.org/10.1007/0-306-47612-6_11.

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Shahid, Azmeh, Kate Wilkinson, Shai Marcu et Colin M. Shapiro. « Frontal Lobe Epilepsy and Parasomnias (FLEP) Scale ». Dans STOP, THAT and One Hundred Other Sleep Scales, 177–78. New York, NY : Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9893-4_38.

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Actes de conférences sur le sujet "Nocturnal Frontal Lobe Epilepsy"

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Pisano, B., B. Cannas, G. Milioli, A. Montisci, F. Pisano, M. Puligheddu, G. Sias et A. Fanni. « Autosomal dominant nocturnal frontal lobe epilepsy seizure characterization through wavelet transform of eeg records and self organizing maps ». Dans 2016 IEEE 26th International Workshop on Machine Learning for Signal Processing (MLSP). IEEE, 2016. http://dx.doi.org/10.1109/mlsp.2016.7738861.

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Yunusov, Valentin, Sergey Demin et Fail Gafarov. « The use of the cross-correlation analysis in the search for diagnostic criteria for nocturnal frontal lobe epilepsy ». Dans Computational Biophysics and Nanobiophotonics, sous la direction de Boris N. Khlebtsov et Dmitry E. Postnov. SPIE, 2022. http://dx.doi.org/10.1117/12.2625879.

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Dorantes, Guadalupe, Martin Mendez, Alfonso Alba, J. S. Gonzalez, Liborio Parrino et G. Milioli. « Heart rate variability in cyclic alternating pattern during sleep in healthy and Nocturnal Front Lobe Epilepsy patients ». Dans 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7319745.

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Delin, Sanja. « 396 Frontal lobe epilepsy with gelastic seizures ». Dans 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.396.

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Bindman, D., J. Foong et P. Thompson. « 50 Predicting psychiatric and cognitive outcomes after surgery for frontal lobe epilepsy ». Dans The British Neuropsychiatry Association – Annual Meeting. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/jnnp-2019-bnpa.50.

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Cuppens, K., L. Lagae, B. Ceulemans, S. Van Huffel et B. Vanrumste. « Detection of nocturnal frontal lobe seizures in pediatric patients by means of accelerometers : A first study ». Dans 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5332557.

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Abbaszadeh, Behrooz, Reza Saadati Fard et Mustapha C. E. Yagoub. « Application of Global Coherence Measure to Characterize Coordinated Neural Activity during Frontal and Temporal Lobe Epilepsy ». Dans 2020 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) in conjunction with the 43rd Annual Conference of the Canadian Medical and Biological Engineering Society. IEEE, 2020. http://dx.doi.org/10.1109/embc44109.2020.9176486.

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