3 recherche sur le mot-clé 'electroencephalogram (EEG)'

Does EEG-neurofeedback improve neurocognitive functioning in children with attention-deficit/hyperactivity disorder? A systematic review and a double-blind placebo-controlled study / Madelon A. VOLLEBREGT in Journal of Child Psychology and Psychiatry, 55-5 (May 2014)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 55-5 (May 2014) . - p.460-472 Titre : Does EEG-neurofeedback improve neurocognitive functioning in children with attention-deficit/hyperactivity disorder? A systematic review and a double-blind placebo-controlled study Type de document : Texte imprimé et/ou numérique Auteurs : Madelon A. VOLLEBREGT, Auteur ; Martine VAN DONGEN-BOOMSMA, Auteur ; Jan K. BUITELAAR, Auteur ; Dorine SLAATS-WILLEMSE, Auteur Article en page(s) : p.460-472 Mots-clés : Neurofeedback  attention-deficit/hyperactivity disorder (ADHD)  randomized controlled trial (RCT)  electroencephalogram (EEG)  efficacy  neurocognition  review Index. décimale : PER Périodiques Résumé : Background The number of placebo-controlled randomized studies relating to EEG-neurofeedback and its effect on neurocognition in attention-deficient/hyperactivity disorder (ADHD) is limited. For this reason, a double blind, randomized, placebo-controlled study was designed to assess the effects of EEG-neurofeedback on neurocognitive functioning in children with ADHD, and a systematic review on this topic was performed. Methods Forty-one children (8–15 years) with a DSM-IV-TR diagnosis of ADHD were randomly allocated to EEG-neurofeedback or placebo-neurofeedback treatment for 30 sessions, twice a week. Children were stratified by age, electrophysiological state of arousal, and medication use. Neurocognitive tests of attention, executive functioning, working memory, and time processing were administered before and after treatment. Researchers, teachers, children and their parents, with the exception of the neurofeedback-therapist, were all blind to treatment assignment. Outcome measures were the changes in neurocognitive performance before and after treatment. Clinical trial registration: www.clinicaltrials.gov: NCT00723684. Results No significant treatment effect on any of the neurocognitive variables was found. A systematic review of the current literature also did not find any systematic beneficial effect of EEG-neurofeedback on neurocognitive functioning. Conclusion Overall, the existing literature and this study fail to support any benefit of neurofeedback on neurocognitive functioning in ADHD, possibly due to small sample sizes and other study limitations. En ligne : http://dx.doi.org/10.1111/jcpp.12143 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=232 [article] Does EEG-neurofeedback improve neurocognitive functioning in children with attention-deficit/hyperactivity disorder? A systematic review and a double-blind placebo-controlled study [Texte imprimé et/ou numérique] / Madelon A. VOLLEBREGT, Auteur ; Martine VAN DONGEN-BOOMSMA, Auteur ; Jan K. BUITELAAR, Auteur ; Dorine SLAATS-WILLEMSE, Auteur . - p.460-472. in Journal of Child Psychology and Psychiatry > 55-5 (May 2014) . - p.460-472 Mots-clés : Neurofeedback  attention-deficit/hyperactivity disorder (ADHD)  randomized controlled trial (RCT)  electroencephalogram (EEG)  efficacy  neurocognition  review Index. décimale : PER Périodiques Résumé : Background The number of placebo-controlled randomized studies relating to EEG-neurofeedback and its effect on neurocognition in attention-deficient/hyperactivity disorder (ADHD) is limited. For this reason, a double blind, randomized, placebo-controlled study was designed to assess the effects of EEG-neurofeedback on neurocognitive functioning in children with ADHD, and a systematic review on this topic was performed. Methods Forty-one children (8–15 years) with a DSM-IV-TR diagnosis of ADHD were randomly allocated to EEG-neurofeedback or placebo-neurofeedback treatment for 30 sessions, twice a week. Children were stratified by age, electrophysiological state of arousal, and medication use. Neurocognitive tests of attention, executive functioning, working memory, and time processing were administered before and after treatment. Researchers, teachers, children and their parents, with the exception of the neurofeedback-therapist, were all blind to treatment assignment. Outcome measures were the changes in neurocognitive performance before and after treatment. Clinical trial registration: www.clinicaltrials.gov: NCT00723684. Results No significant treatment effect on any of the neurocognitive variables was found. A systematic review of the current literature also did not find any systematic beneficial effect of EEG-neurofeedback on neurocognitive functioning. Conclusion Overall, the existing literature and this study fail to support any benefit of neurofeedback on neurocognitive functioning in ADHD, possibly due to small sample sizes and other study limitations. En ligne : http://dx.doi.org/10.1111/jcpp.12143 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=232

Modulation of mu attenuation to social stimuli in children and adults with 16p11.2 deletions and duplications / C. M. HUDAC in Journal of Neurodevelopmental Disorders, 7-1 (December 2015)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 7-1 (December 2015) . - p.25 Titre : Modulation of mu attenuation to social stimuli in children and adults with 16p11.2 deletions and duplications Type de document : Texte imprimé et/ou numérique Auteurs : C. M. HUDAC, Auteur ; A. KRESSE, Auteur ; Benjamin AARONSON, Auteur ; Trent D. DESCHAMPS, Auteur ; S. J. WEBB, Auteur ; Raphael BERNIER, Auteur Article en page(s) : p.25 Langues : Anglais (eng) Mots-clés : 16p11.2  Autism spectrum disorder (ASD)  Copy number variation (CNV)  Electroencephalogram (EEG)  Molecular subtyping  Mu attenuation  Social perception Index. décimale : PER Périodiques Résumé : BACKGROUND: Copy number variations (CNV) within the recurrent ~600 kb chromosomal locus of 16p11.2 are associated with a wide range of neurodevelopmental disorders, including autism spectrum disorder (ASD). However, little is known about the social brain phenotype of 16p11.2 CNV and how this phenotype is related to the social impairments associated with CNVs at this locus. The aim of this preliminary study was to use molecular subtyping to establish the social brain phenotype of individuals with 16p11.2 CNV and how these patterns relate to typical development and ASD. METHODS: We evaluated the social brain phenotype as expressed by mu attenuation in 48 children and adults characterized as duplication carriers (n = 12), deletion carriers (n = 12), individuals with idiopathic ASD (n = 8), and neurotypical controls (n = 16). Participants watched videos containing social and nonsocial motion during electroencephalogram (EEG) acquisition. RESULTS: Overall, only the typical group exhibited predicted patterns of mu modulation to social information (e.g., greater mu attenuation for social than nonsocial motion). Both 16p11.2 CNV groups exhibited more mu attenuation for nonsocial than social motion. The ASD group did not discriminate between conditions and demonstrated less mu attenuation compared to the typical and duplication carriers. Single-trial analysis indicated that mu attenuation decreased over time more rapidly for 16p11.2 CNV groups than the typical group. The duplication group did not diverge from typical patterns of mu attenuation until after initial exposure. CONCLUSIONS: These results indicate atypical but unique patterns of mu attenuation for deletion and duplication carriers, highlighting the need to continue characterizing the social brain phenotype associated with 16p11.2 CNVs. En ligne : http://dx.doi.org/10.1186/s11689-015-9118-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=347 [article] Modulation of mu attenuation to social stimuli in children and adults with 16p11.2 deletions and duplications [Texte imprimé et/ou numérique] / C. M. HUDAC, Auteur ; A. KRESSE, Auteur ; Benjamin AARONSON, Auteur ; Trent D. DESCHAMPS, Auteur ; S. J. WEBB, Auteur ; Raphael BERNIER, Auteur . - p.25. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 7-1 (December 2015) . - p.25 Mots-clés : 16p11.2  Autism spectrum disorder (ASD)  Copy number variation (CNV)  Electroencephalogram (EEG)  Molecular subtyping  Mu attenuation  Social perception Index. décimale : PER Périodiques Résumé : BACKGROUND: Copy number variations (CNV) within the recurrent ~600 kb chromosomal locus of 16p11.2 are associated with a wide range of neurodevelopmental disorders, including autism spectrum disorder (ASD). However, little is known about the social brain phenotype of 16p11.2 CNV and how this phenotype is related to the social impairments associated with CNVs at this locus. The aim of this preliminary study was to use molecular subtyping to establish the social brain phenotype of individuals with 16p11.2 CNV and how these patterns relate to typical development and ASD. METHODS: We evaluated the social brain phenotype as expressed by mu attenuation in 48 children and adults characterized as duplication carriers (n = 12), deletion carriers (n = 12), individuals with idiopathic ASD (n = 8), and neurotypical controls (n = 16). Participants watched videos containing social and nonsocial motion during electroencephalogram (EEG) acquisition. RESULTS: Overall, only the typical group exhibited predicted patterns of mu modulation to social information (e.g., greater mu attenuation for social than nonsocial motion). Both 16p11.2 CNV groups exhibited more mu attenuation for nonsocial than social motion. The ASD group did not discriminate between conditions and demonstrated less mu attenuation compared to the typical and duplication carriers. Single-trial analysis indicated that mu attenuation decreased over time more rapidly for 16p11.2 CNV groups than the typical group. The duplication group did not diverge from typical patterns of mu attenuation until after initial exposure. CONCLUSIONS: These results indicate atypical but unique patterns of mu attenuation for deletion and duplication carriers, highlighting the need to continue characterizing the social brain phenotype associated with 16p11.2 CNVs. En ligne : http://dx.doi.org/10.1186/s11689-015-9118-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=347

Neural Correlates of Sensory Hyporesponsiveness in Toddlers at High Risk for Autism Spectrum Disorder / David M. SIMON in Journal of Autism and Developmental Disorders, 47-9 (September 2017)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 47-9 (September 2017) . - p.2710-2722 Titre : Neural Correlates of Sensory Hyporesponsiveness in Toddlers at High Risk for Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : David M. SIMON, Auteur ; Cara R. DAMIANO, Auteur ; Tiffany G. WOYNAROSKI, Auteur ; Lisa V. IBANEZ, Auteur ; Michael MURIAS, Auteur ; Wendy L. STONE, Auteur ; Mark T. WALLACE, Auteur ; Carissa J. CASCIO, Auteur Article en page(s) : p.2710-2722 Langues : Anglais (eng) Mots-clés : Autism spectrum disorder Infant siblings  Electroencephalogram (EEG)  Functional connectivity  Frontal EEG asymmetry  Sensory hyporesponsiveness Index. décimale : PER Périodiques Résumé : Altered patterns of sensory responsiveness are a frequently reported feature of Autism Spectrum Disorder (ASD). Younger siblings of individuals with ASD are at a greatly elevated risk of a future diagnosis of ASD, but little is known about the neural basis of sensory responsiveness patterns in this population. Younger siblings (n?=?20) of children diagnosed with ASD participated in resting electroencephalography (EEG) at an age of 18 months. Data on toddlers’ sensory responsiveness were obtained using the Sensory Experiences Questionnaire. Correlations were present between hyporesponsiveness and patterns of oscillatory power, functional connectivity, and signal complexity. Our findings suggest that neural signal features hold promise for facilitating early identification and targeted remediation in young children at risk for ASD. En ligne : https://doi.org/10.1007/s10803-017-3191-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=315 [article] Neural Correlates of Sensory Hyporesponsiveness in Toddlers at High Risk for Autism Spectrum Disorder [Texte imprimé et/ou numérique] / David M. SIMON, Auteur ; Cara R. DAMIANO, Auteur ; Tiffany G. WOYNAROSKI, Auteur ; Lisa V. IBANEZ, Auteur ; Michael MURIAS, Auteur ; Wendy L. STONE, Auteur ; Mark T. WALLACE, Auteur ; Carissa J. CASCIO, Auteur . - p.2710-2722. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 47-9 (September 2017) . - p.2710-2722 Mots-clés : Autism spectrum disorder Infant siblings  Electroencephalogram (EEG)  Functional connectivity  Frontal EEG asymmetry  Sensory hyporesponsiveness Index. décimale : PER Périodiques Résumé : Altered patterns of sensory responsiveness are a frequently reported feature of Autism Spectrum Disorder (ASD). Younger siblings of individuals with ASD are at a greatly elevated risk of a future diagnosis of ASD, but little is known about the neural basis of sensory responsiveness patterns in this population. Younger siblings (n?=?20) of children diagnosed with ASD participated in resting electroencephalography (EEG) at an age of 18 months. Data on toddlers’ sensory responsiveness were obtained using the Sensory Experiences Questionnaire. Correlations were present between hyporesponsiveness and patterns of oscillatory power, functional connectivity, and signal complexity. Our findings suggest that neural signal features hold promise for facilitating early identification and targeted remediation in young children at risk for ASD. En ligne : https://doi.org/10.1007/s10803-017-3191-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=315