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Multisensory processing in children with autism: high-density electrical mapping of auditory–somatosensory integration / Natalie RUSSO in Autism Research, 3-5 (October 2010)
[article]
Titre : Multisensory processing in children with autism: high-density electrical mapping of auditory–somatosensory integration Type de document : Texte imprimé et/ou numérique Auteurs : Natalie RUSSO, Auteur ; John J. FOXE, Auteur ; Alice B. BRANDWEIN, Auteur ; Ted ALTSCHULER, Auteur ; Hilary GOMES, Auteur ; Sophie MOLHOLM, Auteur Année de publication : 2010 Article en page(s) : p.253-267 Langues : Anglais (eng) Mots-clés : autism spectrum disorders electrophysiology multisensory integration auditory processing somatosensory processing development Index. décimale : PER Périodiques Résumé : Successful integration of signals from the various sensory systems is crucial for normal sensory–perceptual functioning, allowing for the perception of coherent objects rather than a disconnected cluster of fragmented features. Several prominent theories of autism suggest that automatic integration is impaired in this population, but there have been few empirical tests of this thesis. A standard electrophysiological metric of multisensory integration (MSI) was used to test the integrity of auditory–somatosensory integration in children with autism (N=17, aged 6–16 years), compared to age- and IQ-matched typically developing (TD) children. High-density electrophysiology was recorded while participants were presented with either auditory or somatosensory stimuli alone (unisensory conditions), or as a combined auditory–somatosensory stimulus (multisensory condition), in randomized order. Participants watched a silent movie during testing, ignoring concurrent stimulation. Significant differences between neural responses to the multisensory auditory–somatosensory stimulus and the unisensory stimuli (the sum of the responses to the auditory and somatosensory stimuli when presented alone) served as the dependent measure. The data revealed group differences in the integration of auditory and somatosensory information that appeared at around 175 ms, and were characterized by the presence of MSI for the TD but not the autism spectrum disorder (ASD) children. Overall, MSI was less extensive in the ASD group. These findings are discussed within the framework of current knowledge of MSI in typical development as well as in relation to theories of ASD. En ligne : http://dx.doi.org/10.1002/aur.152 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=115
in Autism Research > 3-5 (October 2010) . - p.253-267[article] Multisensory processing in children with autism: high-density electrical mapping of auditory–somatosensory integration [Texte imprimé et/ou numérique] / Natalie RUSSO, Auteur ; John J. FOXE, Auteur ; Alice B. BRANDWEIN, Auteur ; Ted ALTSCHULER, Auteur ; Hilary GOMES, Auteur ; Sophie MOLHOLM, Auteur . - 2010 . - p.253-267.
Langues : Anglais (eng)
in Autism Research > 3-5 (October 2010) . - p.253-267
Mots-clés : autism spectrum disorders electrophysiology multisensory integration auditory processing somatosensory processing development Index. décimale : PER Périodiques Résumé : Successful integration of signals from the various sensory systems is crucial for normal sensory–perceptual functioning, allowing for the perception of coherent objects rather than a disconnected cluster of fragmented features. Several prominent theories of autism suggest that automatic integration is impaired in this population, but there have been few empirical tests of this thesis. A standard electrophysiological metric of multisensory integration (MSI) was used to test the integrity of auditory–somatosensory integration in children with autism (N=17, aged 6–16 years), compared to age- and IQ-matched typically developing (TD) children. High-density electrophysiology was recorded while participants were presented with either auditory or somatosensory stimuli alone (unisensory conditions), or as a combined auditory–somatosensory stimulus (multisensory condition), in randomized order. Participants watched a silent movie during testing, ignoring concurrent stimulation. Significant differences between neural responses to the multisensory auditory–somatosensory stimulus and the unisensory stimuli (the sum of the responses to the auditory and somatosensory stimuli when presented alone) served as the dependent measure. The data revealed group differences in the integration of auditory and somatosensory information that appeared at around 175 ms, and were characterized by the presence of MSI for the TD but not the autism spectrum disorder (ASD) children. Overall, MSI was less extensive in the ASD group. These findings are discussed within the framework of current knowledge of MSI in typical development as well as in relation to theories of ASD. En ligne : http://dx.doi.org/10.1002/aur.152 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=115 Neurophysiological Indices of Atypical Auditory Processing and Multisensory Integration are Associated with Symptom Severity in Autism / Alice B. BRANDWEIN in Journal of Autism and Developmental Disorders, 45-1 (January 2015)
[article]
Titre : Neurophysiological Indices of Atypical Auditory Processing and Multisensory Integration are Associated with Symptom Severity in Autism Type de document : Texte imprimé et/ou numérique Auteurs : Alice B. BRANDWEIN, Auteur ; John J. FOXE, Auteur ; John S. BUTLER, Auteur ; Hans-Peter FREY, Auteur ; Juliana C. BATES, Auteur ; Lisa H. SHULMAN, Auteur ; Sophie MOLHOLM, Auteur Article en page(s) : p.230-244 Langues : Anglais (eng) Mots-clés : Electrophysiology ERP ASD Multisensory integration ADOS Sensory Profile Index. décimale : PER Périodiques Résumé : Atypical processing and integration of sensory inputs are hypothesized to play a role in unusual sensory reactions and social-cognitive deficits in autism spectrum disorder (ASD). Reports on the relationship between objective metrics of sensory processing and clinical symptoms, however, are surprisingly sparse. Here we examined the relationship between neurophysiological assays of sensory processing and (1) autism severity and (2) sensory sensitivities, in individuals with ASD aged 6–17. Multiple linear regression indicated significant associations between neural markers of auditory processing and multisensory integration, and autism severity. No such relationships were apparent for clinical measures of visual/auditory sensitivities. These data support that aberrant early sensory processing contributes to autism symptoms, and reveal the potential of electrophysiology to objectively subtype autism. En ligne : http://dx.doi.org/10.1007/s10803-014-2212-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=258
in Journal of Autism and Developmental Disorders > 45-1 (January 2015) . - p.230-244[article] Neurophysiological Indices of Atypical Auditory Processing and Multisensory Integration are Associated with Symptom Severity in Autism [Texte imprimé et/ou numérique] / Alice B. BRANDWEIN, Auteur ; John J. FOXE, Auteur ; John S. BUTLER, Auteur ; Hans-Peter FREY, Auteur ; Juliana C. BATES, Auteur ; Lisa H. SHULMAN, Auteur ; Sophie MOLHOLM, Auteur . - p.230-244.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 45-1 (January 2015) . - p.230-244
Mots-clés : Electrophysiology ERP ASD Multisensory integration ADOS Sensory Profile Index. décimale : PER Périodiques Résumé : Atypical processing and integration of sensory inputs are hypothesized to play a role in unusual sensory reactions and social-cognitive deficits in autism spectrum disorder (ASD). Reports on the relationship between objective metrics of sensory processing and clinical symptoms, however, are surprisingly sparse. Here we examined the relationship between neurophysiological assays of sensory processing and (1) autism severity and (2) sensory sensitivities, in individuals with ASD aged 6–17. Multiple linear regression indicated significant associations between neural markers of auditory processing and multisensory integration, and autism severity. No such relationships were apparent for clinical measures of visual/auditory sensitivities. These data support that aberrant early sensory processing contributes to autism symptoms, and reveal the potential of electrophysiology to objectively subtype autism. En ligne : http://dx.doi.org/10.1007/s10803-014-2212-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=258 Acamprosate in a mouse model of fragile X syndrome: modulation of spontaneous cortical activity, ERK1/2 activation, locomotor behavior, and anxiety / T. L. SCHAEFER in Journal of Neurodevelopmental Disorders, 9-1 (December 2017)
[article]
Titre : Acamprosate in a mouse model of fragile X syndrome: modulation of spontaneous cortical activity, ERK1/2 activation, locomotor behavior, and anxiety Type de document : Texte imprimé et/ou numérique Auteurs : T. L. SCHAEFER, Auteur ; M. H. DAVENPORT, Auteur ; L. M. GRAINGER, Auteur ; C. K. ROBINSON, Auteur ; A. T. EARNHEART, Auteur ; M. S. STEGMAN, Auteur ; A. L. LANG, Auteur ; A. ASHWORTH, Auteur ; G. MOLINARO, Auteur ; K. M. HUBER, Auteur ; C. A. ERICKSON, Auteur Article en page(s) : p.6 Langues : Anglais (eng) Mots-clés : Anxiety Dendritic spine density Electrophysiology Extracellular signal-related kinase Fragile X syndrome Hippocampus Hyperactivity Open field Striatum Index. décimale : PER Périodiques Résumé : BACKGROUND: Fragile X Syndrome (FXS) occurs as a result of a silenced fragile X mental retardation 1 gene (FMR1) and subsequent loss of fragile X mental retardation protein (FMRP) expression. Loss of FMRP alters excitatory/inhibitory signaling balance, leading to increased neuronal hyperexcitability and altered behavior. Acamprosate (the calcium salt of N-acetylhomotaurinate), a drug FDA-approved for relapse prevention in the treatment of alcohol dependence in adults, is a novel agent with multiple mechanisms that may be beneficial for people with FXS. There are questions regarding the neuroactive effects of acamprosate and the significance of the molecule's calcium moiety. Therefore, the electrophysiological, cellular, molecular, and behavioral effects of acamprosate were assessed in the Fmr1(-/y) (knock out; KO) mouse model of FXS controlling for the calcium salt in several experiments. METHODS: Fmr1 KO mice and their wild-type (WT) littermates were utilized to assess acamprosate treatment on cortical UP state parameters, dendritic spine density, and seizure susceptibility. Brain extracellular-signal regulated kinase 1/2 (ERK1/2) activation was used to investigate this signaling molecule as a potential biomarker for treatment response. Additional adult mice were used to assess chronic acamprosate treatment and any potential effects of the calcium moiety using CaCl2 treatment on behavior and nuclear ERK1/2 activation. RESULTS: Acamprosate attenuated prolonged cortical UP state duration, decreased elevated ERK1/2 activation in brain tissue, and reduced nuclear ERK1/2 activation in the dentate gyrus in KO mice. Acamprosate treatment modified behavior in anxiety and locomotor tests in Fmr1 KO mice in which control-treated KO mice were shown to deviate from control-treated WT mice. Mice treated with CaCl2 were not different from saline-treated mice in the adult behavior battery or nuclear ERK1/2 activation. CONCLUSIONS: These data indicate that acamprosate, and not calcium, improves function reminiscent of reduced anxiety-like behavior and hyperactivity in Fmr1 KO mice and that acamprosate attenuates select electrophysiological and molecular dysregulation that may play a role in the pathophysiology of FXS. Differences between control-treated KO and WT mice were not evident in a recognition memory test or in examination of acoustic startle response/prepulse inhibition which impeded conclusions from being made about the treatment effects of acamprosate in these instances. En ligne : http://dx.doi.org/10.1186/s11689-017-9184-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=349
in Journal of Neurodevelopmental Disorders > 9-1 (December 2017) . - p.6[article] Acamprosate in a mouse model of fragile X syndrome: modulation of spontaneous cortical activity, ERK1/2 activation, locomotor behavior, and anxiety [Texte imprimé et/ou numérique] / T. L. SCHAEFER, Auteur ; M. H. DAVENPORT, Auteur ; L. M. GRAINGER, Auteur ; C. K. ROBINSON, Auteur ; A. T. EARNHEART, Auteur ; M. S. STEGMAN, Auteur ; A. L. LANG, Auteur ; A. ASHWORTH, Auteur ; G. MOLINARO, Auteur ; K. M. HUBER, Auteur ; C. A. ERICKSON, Auteur . - p.6.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 9-1 (December 2017) . - p.6
Mots-clés : Anxiety Dendritic spine density Electrophysiology Extracellular signal-related kinase Fragile X syndrome Hippocampus Hyperactivity Open field Striatum Index. décimale : PER Périodiques Résumé : BACKGROUND: Fragile X Syndrome (FXS) occurs as a result of a silenced fragile X mental retardation 1 gene (FMR1) and subsequent loss of fragile X mental retardation protein (FMRP) expression. Loss of FMRP alters excitatory/inhibitory signaling balance, leading to increased neuronal hyperexcitability and altered behavior. Acamprosate (the calcium salt of N-acetylhomotaurinate), a drug FDA-approved for relapse prevention in the treatment of alcohol dependence in adults, is a novel agent with multiple mechanisms that may be beneficial for people with FXS. There are questions regarding the neuroactive effects of acamprosate and the significance of the molecule's calcium moiety. Therefore, the electrophysiological, cellular, molecular, and behavioral effects of acamprosate were assessed in the Fmr1(-/y) (knock out; KO) mouse model of FXS controlling for the calcium salt in several experiments. METHODS: Fmr1 KO mice and their wild-type (WT) littermates were utilized to assess acamprosate treatment on cortical UP state parameters, dendritic spine density, and seizure susceptibility. Brain extracellular-signal regulated kinase 1/2 (ERK1/2) activation was used to investigate this signaling molecule as a potential biomarker for treatment response. Additional adult mice were used to assess chronic acamprosate treatment and any potential effects of the calcium moiety using CaCl2 treatment on behavior and nuclear ERK1/2 activation. RESULTS: Acamprosate attenuated prolonged cortical UP state duration, decreased elevated ERK1/2 activation in brain tissue, and reduced nuclear ERK1/2 activation in the dentate gyrus in KO mice. Acamprosate treatment modified behavior in anxiety and locomotor tests in Fmr1 KO mice in which control-treated KO mice were shown to deviate from control-treated WT mice. Mice treated with CaCl2 were not different from saline-treated mice in the adult behavior battery or nuclear ERK1/2 activation. CONCLUSIONS: These data indicate that acamprosate, and not calcium, improves function reminiscent of reduced anxiety-like behavior and hyperactivity in Fmr1 KO mice and that acamprosate attenuates select electrophysiological and molecular dysregulation that may play a role in the pathophysiology of FXS. Differences between control-treated KO and WT mice were not evident in a recognition memory test or in examination of acoustic startle response/prepulse inhibition which impeded conclusions from being made about the treatment effects of acamprosate in these instances. En ligne : http://dx.doi.org/10.1186/s11689-017-9184-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=349 Cortical neurons derived from human pluripotent stem cells lacking FMRP display altered spontaneous firing patterns / Shreya DAS SHARMA in Molecular Autism, 11 (2020)
[article]
Titre : Cortical neurons derived from human pluripotent stem cells lacking FMRP display altered spontaneous firing patterns Type de document : Texte imprimé et/ou numérique Auteurs : Shreya DAS SHARMA, Auteur ; Rakhi PAL, Auteur ; Bharath Kumar REDDY, Auteur ; Bhuvaneish T. SELVARAJ, Auteur ; Nisha RAJ, Auteur ; Krishna Kumar SAMAGA, Auteur ; Durga J. SRINIVASAN, Auteur ; Loren ORNELAS, Auteur ; Dhruv SAREEN, Auteur ; Matthew R. LIVESEY, Auteur ; Gary J. BASSELL, Auteur ; Clive N. SVENDSEN, Auteur ; Peter C. KIND, Auteur ; Siddharthan CHANDRAN, Auteur ; Sumantra CHATTARJI, Auteur ; David J. A. WYLLIE, Auteur Article en page(s) : 52 p. Langues : Anglais (eng) Mots-clés : Action potential Disease-modelling Electrophysiology Fragile X syndrome Index. décimale : PER Périodiques Résumé : BACKGROUND: Fragile X syndrome (FXS), a neurodevelopmental disorder, is a leading monogenetic cause of intellectual disability and autism spectrum disorder. Notwithstanding the extensive studies using rodent and other pre-clinical models of FXS, which have provided detailed mechanistic insights into the pathophysiology of this disorder, it is only relatively recently that human stem cell-derived neurons have been employed as a model system to further our understanding of the pathophysiological events that may underlie FXS. Our study assesses the physiological properties of human pluripotent stem cell-derived cortical neurons lacking fragile X mental retardation protein (FMRP). METHODS: Electrophysiological whole-cell voltage- and current-clamp recordings were performed on two control and three FXS patient lines of human cortical neurons derived from induced pluripotent stem cells. In addition, we also describe the properties of an isogenic pair of lines in one of which FMR1 gene expression has been silenced. RESULTS: Neurons lacking FMRP displayed bursts of spontaneous action potential firing that were more frequent but shorter in duration compared to those recorded from neurons expressing FMRP. Inhibition of large conductance Ca(2+)-activated K(+) currents and the persistent Na(+) current in control neurons phenocopies action potential bursting observed in neurons lacking FMRP, while in neurons lacking FMRP pharmacological potentiation of voltage-dependent Na(+) channels phenocopies action potential bursting observed in control neurons. Notwithstanding the changes in spontaneous action potential firing, we did not observe any differences in the intrinsic properties of neurons in any of the lines examined. Moreover, we did not detect any differences in the properties of miniature excitatory postsynaptic currents in any of the lines. CONCLUSIONS: Pharmacological manipulations can alter the action potential burst profiles in both control and FMRP-null human cortical neurons, making them appear like their genetic counterpart. Our studies indicate that FMRP targets that have been found in rodent models of FXS are also potential targets in a human-based model system, and we suggest potential mechanisms by which activity is altered. En ligne : http://dx.doi.org/10.1186/s13229-020-00351-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427
in Molecular Autism > 11 (2020) . - 52 p.[article] Cortical neurons derived from human pluripotent stem cells lacking FMRP display altered spontaneous firing patterns [Texte imprimé et/ou numérique] / Shreya DAS SHARMA, Auteur ; Rakhi PAL, Auteur ; Bharath Kumar REDDY, Auteur ; Bhuvaneish T. SELVARAJ, Auteur ; Nisha RAJ, Auteur ; Krishna Kumar SAMAGA, Auteur ; Durga J. SRINIVASAN, Auteur ; Loren ORNELAS, Auteur ; Dhruv SAREEN, Auteur ; Matthew R. LIVESEY, Auteur ; Gary J. BASSELL, Auteur ; Clive N. SVENDSEN, Auteur ; Peter C. KIND, Auteur ; Siddharthan CHANDRAN, Auteur ; Sumantra CHATTARJI, Auteur ; David J. A. WYLLIE, Auteur . - 52 p.
Langues : Anglais (eng)
in Molecular Autism > 11 (2020) . - 52 p.
Mots-clés : Action potential Disease-modelling Electrophysiology Fragile X syndrome Index. décimale : PER Périodiques Résumé : BACKGROUND: Fragile X syndrome (FXS), a neurodevelopmental disorder, is a leading monogenetic cause of intellectual disability and autism spectrum disorder. Notwithstanding the extensive studies using rodent and other pre-clinical models of FXS, which have provided detailed mechanistic insights into the pathophysiology of this disorder, it is only relatively recently that human stem cell-derived neurons have been employed as a model system to further our understanding of the pathophysiological events that may underlie FXS. Our study assesses the physiological properties of human pluripotent stem cell-derived cortical neurons lacking fragile X mental retardation protein (FMRP). METHODS: Electrophysiological whole-cell voltage- and current-clamp recordings were performed on two control and three FXS patient lines of human cortical neurons derived from induced pluripotent stem cells. In addition, we also describe the properties of an isogenic pair of lines in one of which FMR1 gene expression has been silenced. RESULTS: Neurons lacking FMRP displayed bursts of spontaneous action potential firing that were more frequent but shorter in duration compared to those recorded from neurons expressing FMRP. Inhibition of large conductance Ca(2+)-activated K(+) currents and the persistent Na(+) current in control neurons phenocopies action potential bursting observed in neurons lacking FMRP, while in neurons lacking FMRP pharmacological potentiation of voltage-dependent Na(+) channels phenocopies action potential bursting observed in control neurons. Notwithstanding the changes in spontaneous action potential firing, we did not observe any differences in the intrinsic properties of neurons in any of the lines examined. Moreover, we did not detect any differences in the properties of miniature excitatory postsynaptic currents in any of the lines. CONCLUSIONS: Pharmacological manipulations can alter the action potential burst profiles in both control and FMRP-null human cortical neurons, making them appear like their genetic counterpart. Our studies indicate that FMRP targets that have been found in rodent models of FXS are also potential targets in a human-based model system, and we suggest potential mechanisms by which activity is altered. En ligne : http://dx.doi.org/10.1186/s13229-020-00351-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427 Electroencephalographic spectral power as a marker of cortical function and disease severity in girls with Rett syndrome / K. J. ROCHE in Journal of Neurodevelopmental Disorders, 11-1 (December 2019)
[article]
Titre : Electroencephalographic spectral power as a marker of cortical function and disease severity in girls with Rett syndrome Type de document : Texte imprimé et/ou numérique Auteurs : K. J. ROCHE, Auteur ; J. J. LEBLANC, Auteur ; A. R. LEVIN, Auteur ; H. M. O'LEARY, Auteur ; L. M. BACZEWSKI, Auteur ; C. A. NELSON, Auteur Article en page(s) : 15 p. Langues : Anglais (eng) Mots-clés : Biomarker Eeg Electroencephalography Electrophysiology Rett syndrome Spectral power Index. décimale : PER Périodiques Résumé : BACKGROUND: Rett syndrome is a neurodevelopmental disorder caused by a mutation in the X-linked MECP2 gene. Individuals with Rett syndrome typically develop normally until around 18 months of age before undergoing a developmental regression, and the disorder can lead to cognitive, motor, sensory, and autonomic dysfunction. Understanding the mechanism of developmental regression represents a unique challenge when viewed through a neuroscience lens. Are circuits that were previously established erased, and are new ones built to supplant old ones? One way to examine circuit-level changes is with the use of electroencephalography (EEG). Previous studies of the EEG in individuals with Rett syndrome have focused on morphological characteristics, but few have explored spectral power, including power as an index of brain function or disease severity. This study sought to determine if EEG power differs in girls with Rett syndrome and typically developing girls and among girls with Rett syndrome based on various clinical characteristics in order to better understand neural connectivity and cortical organization in individuals with this disorder. METHODS: Resting state EEG data were acquired from girls with Rett syndrome (n = 57) and typically developing children without Rett syndrome (n = 37). Clinical data were also collected for girls with Rett syndrome. EEG power across several brain regions in numerous frequency bands was then compared between girls with Rett syndrome and typically developing children and power in girls with Rett syndrome was compared based on these clinical measures. 1/f slope was also compared between groups. RESULTS: Girls with Rett syndrome demonstrate significantly lower power in the middle frequency bands across multiple brain regions. Additionally, girls with Rett syndrome that are postregression demonstrate significantly higher power in the lower frequency delta and theta bands and a significantly more negative slope of the power spectrum. Increased power in these bands, as well as a more negative 1/f slope, trended with lower cognitive assessment scores. CONCLUSIONS: Increased power in lower frequency bands is consistent with previous studies demonstrating a "slowing" of the background EEG in Rett syndrome. This increase, particularly in the delta band, could represent abnormal cortical inhibition due to dysfunctional GABAergic signaling and could potentially be used as a marker of severity due to associations with more severe Rett syndrome phenotypes. En ligne : https://dx.doi.org/10.1186/s11689-019-9275-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409
in Journal of Neurodevelopmental Disorders > 11-1 (December 2019) . - 15 p.[article] Electroencephalographic spectral power as a marker of cortical function and disease severity in girls with Rett syndrome [Texte imprimé et/ou numérique] / K. J. ROCHE, Auteur ; J. J. LEBLANC, Auteur ; A. R. LEVIN, Auteur ; H. M. O'LEARY, Auteur ; L. M. BACZEWSKI, Auteur ; C. A. NELSON, Auteur . - 15 p.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 11-1 (December 2019) . - 15 p.
Mots-clés : Biomarker Eeg Electroencephalography Electrophysiology Rett syndrome Spectral power Index. décimale : PER Périodiques Résumé : BACKGROUND: Rett syndrome is a neurodevelopmental disorder caused by a mutation in the X-linked MECP2 gene. Individuals with Rett syndrome typically develop normally until around 18 months of age before undergoing a developmental regression, and the disorder can lead to cognitive, motor, sensory, and autonomic dysfunction. Understanding the mechanism of developmental regression represents a unique challenge when viewed through a neuroscience lens. Are circuits that were previously established erased, and are new ones built to supplant old ones? One way to examine circuit-level changes is with the use of electroencephalography (EEG). Previous studies of the EEG in individuals with Rett syndrome have focused on morphological characteristics, but few have explored spectral power, including power as an index of brain function or disease severity. This study sought to determine if EEG power differs in girls with Rett syndrome and typically developing girls and among girls with Rett syndrome based on various clinical characteristics in order to better understand neural connectivity and cortical organization in individuals with this disorder. METHODS: Resting state EEG data were acquired from girls with Rett syndrome (n = 57) and typically developing children without Rett syndrome (n = 37). Clinical data were also collected for girls with Rett syndrome. EEG power across several brain regions in numerous frequency bands was then compared between girls with Rett syndrome and typically developing children and power in girls with Rett syndrome was compared based on these clinical measures. 1/f slope was also compared between groups. RESULTS: Girls with Rett syndrome demonstrate significantly lower power in the middle frequency bands across multiple brain regions. Additionally, girls with Rett syndrome that are postregression demonstrate significantly higher power in the lower frequency delta and theta bands and a significantly more negative slope of the power spectrum. Increased power in these bands, as well as a more negative 1/f slope, trended with lower cognitive assessment scores. CONCLUSIONS: Increased power in lower frequency bands is consistent with previous studies demonstrating a "slowing" of the background EEG in Rett syndrome. This increase, particularly in the delta band, could represent abnormal cortical inhibition due to dysfunctional GABAergic signaling and could potentially be used as a marker of severity due to associations with more severe Rett syndrome phenotypes. En ligne : https://dx.doi.org/10.1186/s11689-019-9275-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 Event-related potential (ERP) correlates of face processing in verbal children with autism spectrum disorders (ASD) and their first-degree relatives: a family study / O. V. SYSOEVA in Molecular Autism, 9 (2018)
PermalinkGuidelines and Best Practices for Electrophysiological Data Collection, Analysis and Reporting in Autism / Sara Jane WEBB in Journal of Autism and Developmental Disorders, 45-2 (February 2015)
PermalinkKnockout of NMDA Receptors in Parvalbumin Interneurons Recreates Autism-Like Phenotypes / John A. SAUNDERS in Autism Research, 6-2 (April 2013)
PermalinkMeasures of tonic and phasic activity of the locus coeruleus-norepinephrine system in children with autism spectrum disorder: An event-related potential and pupillometry study / Yesol KIM in Autism Research, 15-12 (December 2022)
PermalinkMotivational incentives and methylphenidate enhance electrophysiological correlates of error monitoring in children with attention deficit/hyperactivity disorder / Madeleine J. GROOM in Journal of Child Psychology and Psychiatry, 54-8 (August 2013)
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