Academic literature on the topic 'Epilepsy, Nocturnal Frontal Lobe Epilepsy, Febrile Seizures'
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Journal articles on the topic "Epilepsy, Nocturnal Frontal Lobe Epilepsy, Febrile Seizures"
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Jiang, Yongning, and Xiangqin Zhou. "Frontal lobe epilepsy manifesting as vertigo: a case report and literature review." Journal of International Medical Research 48, no. 9 (September 2020): 030006052094616. http://dx.doi.org/10.1177/0300060520946166.
Full textAbstract:
Frontal lobe epilepsy is a common neurological disorder with a broad spectrum of symptoms. Frontal lobe epilepsy presenting with vertigo is extremely rare, and the relevant pathogenesis remains unclear. Herein, we report a case of frontal lobe epilepsy manifesting as vertigo, and we review the relevant literature. A 34-year-old woman presented with a 10-year history of general tonic–clonic seizures. In the month prior to admission, she experienced nocturnal seizures on two occasions. Video electroencephalogram monitoring showed frequent clinical seizures during which the patient felt transient vertigo. The ictal electroencephalogram revealed a medium-amplitude spike and slow wave complex originating from the frontal lobes. The patient was treated with oral sodium valproate, levetiracetam, and lamotrigine. After a 6-month follow-up period, her seizures were well controlled. Our findings expand the symptom spectrum of epilepsy, suggesting that vertigo can be an uncommon clinical manifestation of frontal lobe epilepsy. Although the pathological correlation between vertigo and epilepsy remains elusive, our findings indicate that vestibular cortical neurons may participate in periodic epileptiform discharges of the frontal lobe. Clinicians should be aware of a potential diagnosis of epilepsy in patients presenting with vertigo as the onset symptom because this condition is usually underdiagnosed.
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Provini, Federica, Pasquale Montagna, Giuseppe Plazzi, and Elio Lugaresi. "Nocturnal frontal lobe epilepsy: A wide spectrum of seizures." Movement Disorders 15, no. 6 (November 2000): 1264. http://dx.doi.org/10.1002/1531-8257(200011)15:6<1264::aid-mds1033>3.0.co;2-4.
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Rathore, Geetanjali, Paul Larsen, Manish Parakh, and Cristina Fernandez. "Choking at Night: A Case of Opercular Nocturnal Frontal Lobe Epilepsy." Case Reports in Pediatrics 2013 (2013): 1–3. http://dx.doi.org/10.1155/2013/606385.
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Frontal lobe seizures have a tendency to occur in sleep and in most cases occur exclusively insleep; these individuals are said to have nocturnal frontal lobe (NFLE). NFLE can be difficult to distinguish clinically from various other sleep disorders, particularly parasomnias, which also present with paroxysmal motor activity in sleep. Interictal and ictal EEG findings are frequently unremarkable or nonspecific in both parasomnias and NFLE making the diagnosis even more difficult. Nocturnal epilepsy should be suspected in patients with paroxysmal events at night characterized by high frequency, repetition, extrapyramidal features, and marked stereotypy of attacks. Here we present a 13-year-old female who was extensively worked up for choking episodes at night. On repeat video EEG she was found to have frontal opercular seizures. Once on Carbamazepine, her seizures completely resolved.
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Alsaleem, Mahdi, Vivien Carrion, Arie Weinstock, and Praveen Chandrasekharan. "Infantile refractory seizures due to de novo KCNT 1 mutation." BMJ Case Reports 12, no. 10 (October 2019): e231178. http://dx.doi.org/10.1136/bcr-2019-231178.
Full textAbstract:
We describe a term female infant who presented with multiple seizures early in infancy. The clinical and electrical seizures were refractory to traditional antiepileptic medications. After extensive workup, seizure panel testing revealed KCNT1 gene mutation, which is associated with nocturnal frontal lobe epilepsy and epilepsy of infancy with migrating focal seizures. The infant’s condition improved with the combination of traditional as well non-traditional antiepileptic therapy.
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El Helou, J., V. Navarro, C. Depienne, E. Fedirko, E. LeGuern, M. Baulac, I. An-Gourfinkel, and C. Adam. "K-complex-induced seizures in autosomal dominant nocturnal frontal lobe epilepsy." Clinical Neurophysiology 119, no. 10 (October 2008): 2201–4. http://dx.doi.org/10.1016/j.clinph.2008.07.212.
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Kanner, Andres M. "Nocturnal Frontal Lobe Epilepsy: There is Bad, Good, and Very Good News!" Epilepsy Currents 7, no. 5 (September 2007): 131–33. http://dx.doi.org/10.1111/j.1535-7511.2007.00200.x.
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Surgical Treatment of Drug-Resistant Nocturnal Frontal Lobe Epilepsy. Nobili L, Francione S, Mai R, Cardinale F, Castana L, Tassi L, Sartori I, Didato G, Citterio A, Colombo N, Galli C, Lo Russo G, Cossu M. Brain 2007;130(Pt 2):561–573. Of the cases with nocturnal frontal lobe epilepsy (NFLE) 30% are refractory to antiepileptic medication, with several patients suffering from the effects of both ongoing seizures and disrupted sleep. From a consecutive series of 522 patients operated on for drug-resistant focal epilepsy, 21 cases (4%), whose frontal lobe seizures occurred almost exclusively (>90%) during sleep, were selected. All patients underwent a comprehensive pre-surgical evaluation, which included history, interictal EEG, scalp video-EEG monitoring, high-resolution MRI and, when indicated, invasive recording by stereo-EEG (SEEG). There were 11 males and 10 females, whose mean age at seizure onset was 6.2 years, mean age at surgery was 24.7 years and seizure frequency ranged from <20/month to >300/month. Nine patients reported excessive daytime sleepiness (EDS). Prevalent ictal clinical signs were represented by asymmetric posturing (6 cases), hyperkinetic automatisms (10 cases), combined tonic posturing and hyperkinetic automatisms (4 cases) and mimetic automatisms (1 case). All patients reported some kind of subjective manifestations. Interictal and ictal EEG provided lateralizing or localizing information in most patients. MRI was unrevealing in 10 cases and it showed a focal anatomical abnormality in one frontal lobe in 11 cases. Eighteen patients underwent a SEEG evaluation to better define the epileptogenic zone (EZ). All patients received a microsurgical resection in one frontal lobe, tailored according to pre-surgical evaluations. Two patients were operated on twice owing to poor results after the first resection. Histology demonstrated a Taylor-type focal cortical dysplasia (FCD) in 16 patients and an architectural FCD in 4. In one case no histological change was found. After a post-operative follow-up of at least 12 months (mean 42.5 months) all the 16 patients with a Taylor's FCD were in Engel's Class Ia and the other 5 patients were in Engel's Classes II or III. After 6 months post-surgery EDS had disappeared in the 9 patients who presented this complaint pre-operatively. It is concluded that patients with drug-resistant, disabling sleep-related seizures of frontal lobe origin should be considered for resective surgery, which may provide excellent results both on seizures and on epilepsy-related sleep disturbances. An accurate pre-surgical evaluation, which often requires invasive EEG recording, is mandatory to define the EZ. Further investigation is needed to explain the possible causal relationships between FCD, particularly Taylor-type, and sleep-related seizures, as observed in this cohort of NFLE patients.
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Mathews, Gregory C. "Is Too Much Inhibition to Blame in Autosomal Dominant Nocturnal Frontal Lobe Epilepsy?" Epilepsy Currents 7, no. 4 (July 2007): 114–16. http://dx.doi.org/10.1111/j.1535-7511.2007.00193.x.
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Seizures and Enhanced Cortical GABAergic Inhibition in Two Mouse Models of Human Autosomal Dominant Nocturnal Frontal Lobe Epilepsy. Klaassen A, Glykys J, Maguire J, Labarca C, Mody I, Boulter J. Proc Natl Acad Sci USA 2006;103(50):19152–19157. Selected mutations in the human α4 or β2 neuronal nicotinic acetylcholine receptor subunit genes cosegregate with a partial epilepsy syndrome known as autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). To examine possible mechanisms underlying this inherited epilepsy, we engineered two ADNFLE mutations ( Chrna4S252F and Chrna4+L264) in mice. Heterozygous ADNFLE mutant mice show persistent, abnormal cortical electroencephalograms with prominent delta and theta frequencies, exhibit frequent spontaneous seizures, and show an increased sensitivity to the proconvulsant action of nicotine. Relative to WT, electrophysiological recordings from ADNFLE mouse layer II/III cortical pyramidal cells reveal a >20-fold increase in nicotine-evoked inhibitory postsynaptic currents with no effect on excitatory postsynaptic currents. i.p. injection of a subthreshold dose of picrotoxin, a use-dependent γ-aminobutyric acid receptor antagonist, reduces cortical electroencephalogram delta power and transiently inhibits spontaneous seizure activity in ADNFLE mutant mice. Our studies suggest that the mechanism underlying ADNFLE seizures may involve inhibitory synchronization of cortical networks via activation of mutant α4-containing nicotinic acetylcholine receptors located on the presynaptic terminals and somatodendritic compartments of cortical GABAergic interneurons.
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Ryvlin, Philippe, Lorella Minotti, Genevieve Demarquay, Edouard Hirsch, Alexis Arzimanoglou, Dominique Hoffman, Marc Guenot, Fabienne Picard, Sylvain Rheims, and Philippe Kahane. "Nocturnal Hypermotor Seizures, Suggesting Frontal Lobe Epilepsy, Can Originate in the Insula." Epilepsia 47, no. 4 (April 2006): 755–65. http://dx.doi.org/10.1111/j.1528-1167.2006.00510.x.
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Pisano, Fabio, Giuliana Sias, Alessandra Fanni, Barbara Cannas, António Dourado, Barbara Pisano, and Cesar A. Teixeira. "Convolutional Neural Network for Seizure Detection of Nocturnal Frontal Lobe Epilepsy." Complexity 2020 (March 31, 2020): 1–10. http://dx.doi.org/10.1155/2020/4825767.
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The Nocturnal Frontal Lobe Epilepsy (NFLE) is a form of epilepsy in which seizures occur predominantly during sleep. In other forms of epilepsy, the commonly used clinical approach mainly involves manual inspection of encephalography (EEG) signals, a laborious and time-consuming process which often requires the contribution of more than one experienced neurologist. In the last decades, numerous approaches to automate this detection have been proposed and, more recently, machine learning has shown very promising performance. In this paper, an original Convolutional Neural Network (CNN) architecture is proposed to develop patient-specific seizure detection models for three patients affected by NFLE. The performances, in terms of accuracy, sensitivity, and specificity, exceed by several percentage points those in the most recent literature. The capability of the patient-specific models has been also tested to compare the obtained seizure onset times with those provided by the neurologists, with encouraging results. Moreover, the same CNN architecture has been used to develop a cross-patient seizure detection system, resorting to the transfer-learning paradigm. Starting from a patient-specific model, few data from a new patient are enough to customize his model. This contribution aims to alleviate the task of neurologists, who may have a robust indication to corroborate their clinical conclusions.
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De Paolis, Fernando, Elena Colizzi, Giulia Milioli, Andrea Grassi, Silvia Riccardi, Monica Puligheddu, Mario Giovanni Terzano, Francesco Marrosu, and Liborio Parrino. "Effects of antiepileptic treatment on sleep and seizures in nocturnal frontal lobe epilepsy." Sleep Medicine 14, no. 7 (July 2013): 597–604. http://dx.doi.org/10.1016/j.sleep.2013.02.014.
Full textDissertations / Theses on the topic "Epilepsy, Nocturnal Frontal Lobe Epilepsy, Febrile Seizures"
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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>. "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.
Full textAbstract:
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>. "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/.
Full textAbstract:
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.
Books on the topic "Epilepsy, Nocturnal Frontal Lobe Epilepsy, Febrile Seizures"
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Nobili, Lino, Paola Proserpio, Steve Gibbs, and Giuseppe Plazzi. Sleep and epilepsy. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and 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.
Book chapters on the topic "Epilepsy, Nocturnal Frontal Lobe Epilepsy, Febrile Seizures"
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Neme-Mercante, Silvia, Zahreddin Alsheikhtaha, and Nancy Foldvary-Schaefer. "Like Clockwork." In Sleep Disorders, 248–73. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190671099.003.0012.
Full textAbstract:
Sleep-related hypermotor epilepsy, previously known as nocturnal frontal lobe epilepsy, is a focal epilepsy with seizures arising from sleep, typically involving activation of ventromesial frontal, insular, or frontoparietal networks. The etiology may be genetic or due to structural pathology but in most cases is unknown. Seizures are characterized by hypermotor activity with violent proximal limb movements or tonic-dystonic posturing, usually short in duration and often in clusters during non–rapid-eye-movement (NREM) sleep and sleep/wake transitions. The differentiation of seizures from physiologically arousals or pathological arousals (NREM parasomnias) is often challenging, and misdiagnosis is common. Video electroencephalography-polysomnography recording typical events is often required to confirm the diagnosis.