An fMRI study of facial emotion processing in children and adolescents with 22q11.2 deletion syndrome / R. AZUMA in Journal of Neurodevelopmental Disorders, 7-1 (December 2015)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 7-1 (December 2015) . - p.1 Titre : An fMRI study of facial emotion processing in children and adolescents with 22q11.2 deletion syndrome Type de document : Texte imprimé et/ou numérique Auteurs : R. AZUMA, Auteur ; Quinton DEELEY, Auteur ; Linda E. CAMPBELL, Auteur ; Eileen DALY, Auteur ; V. GIAMPIETRO, Auteur ; Michael BRAMMER, Auteur ; K. C. MURPHY, Auteur ; D. G. MURPHY, Auteur Article en page(s) : p.1 Langues : Anglais (eng) Mots-clés : 22q11.2 deletion syndrome (22q11DS)  Children  Emotion  Social cognition  Velo-cardio-facial syndrome (VCFS)  fMRI Index. décimale : PER Périodiques Résumé : BACKGROUND: 22q11.2 deletion syndrome (22q11DS, velo-cardio-facial syndrome [VCFS]) is a genetic disorder associated with interstitial deletions of chromosome 22q11.2. In addition to high rates of neuropsychiatric disorders, children with 22q11DS have impairments of face processing, as well as IQ-independent deficits in visuoperceptual function and social and abstract reasoning. These face-processing deficits may contribute to the social impairments of 22q11DS. However, their neurobiological basis is poorly understood. METHODS: We used event-related functional magnetic resonance imaging (fMRI) to examine neural responses when children with 22q11DS (aged 9-17 years) and healthy controls (aged 8-17 years) incidentally processed neutral expressions and mild (50%) and intense (100%) expressions of fear and disgust. We included 28 right-handed children and adolescents: 14 with 22q11DS and 14 healthy (including nine siblings) controls. RESULTS: Within groups, contrasts showed that individuals significantly activated 'face responsive' areas when viewing neutral faces, including fusiform-extrastriate cortices. Further, within both groups, there was a significant positive linear trend in activation of fusiform-extrastriate cortices and cerebellum to increasing intensities of fear. There were, however, also between-group differences. Children with 22q11DS generally showed reduced activity as compared to controls in brain regions involved in social cognition and emotion processing across emotion types and intensities, including fusiform-extrastriate cortices, anterior cingulate cortex (Brodmann area (BA) 24/32), and superomedial prefrontal cortices (BA 6). Also, an exploratory correlation analysis showed that within 22q11DS children reduced activation was associated with behavioural impairment-social difficulties (measured using the Total Difficulties Score from the Strengths and Difficulties Questionnaire [SDQ]) were significantly negatively correlated with brain activity during fear and disgust processing (respectively) in the left precentral gyrus (BA 4) and in the left fusiform gyrus (FG, BA 19), right lingual gyrus (BA 18), and bilateral cerebellum. CONCLUSIONS: Regions involved in face processing, including fusiform-extrastriate cortices, anterior cingulate gyri, and superomedial prefrontal cortices (BA 6), are activated by facial expressions of fearful, disgusted, and neutral expressions in children with 22q11DS but generally to a lesser degree than in controls. Hypoactivation in these regions may partly explain the social impairments of children with 22q11DS. En ligne : http://dx.doi.org/10.1186/1866-1955-7-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=347 [article] An fMRI study of facial emotion processing in children and adolescents with 22q11.2 deletion syndrome [Texte imprimé et/ou numérique] / R. AZUMA, Auteur ; Quinton DEELEY, Auteur ; Linda E. CAMPBELL, Auteur ; Eileen DALY, Auteur ; V. GIAMPIETRO, Auteur ; Michael BRAMMER, Auteur ; K. C. MURPHY, Auteur ; D. G. MURPHY, Auteur . - p.1. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 7-1 (December 2015) . - p.1 Mots-clés : 22q11.2 deletion syndrome (22q11DS)  Children  Emotion  Social cognition  Velo-cardio-facial syndrome (VCFS)  fMRI Index. décimale : PER Périodiques Résumé : BACKGROUND: 22q11.2 deletion syndrome (22q11DS, velo-cardio-facial syndrome [VCFS]) is a genetic disorder associated with interstitial deletions of chromosome 22q11.2. In addition to high rates of neuropsychiatric disorders, children with 22q11DS have impairments of face processing, as well as IQ-independent deficits in visuoperceptual function and social and abstract reasoning. These face-processing deficits may contribute to the social impairments of 22q11DS. However, their neurobiological basis is poorly understood. METHODS: We used event-related functional magnetic resonance imaging (fMRI) to examine neural responses when children with 22q11DS (aged 9-17 years) and healthy controls (aged 8-17 years) incidentally processed neutral expressions and mild (50%) and intense (100%) expressions of fear and disgust. We included 28 right-handed children and adolescents: 14 with 22q11DS and 14 healthy (including nine siblings) controls. RESULTS: Within groups, contrasts showed that individuals significantly activated 'face responsive' areas when viewing neutral faces, including fusiform-extrastriate cortices. Further, within both groups, there was a significant positive linear trend in activation of fusiform-extrastriate cortices and cerebellum to increasing intensities of fear. There were, however, also between-group differences. Children with 22q11DS generally showed reduced activity as compared to controls in brain regions involved in social cognition and emotion processing across emotion types and intensities, including fusiform-extrastriate cortices, anterior cingulate cortex (Brodmann area (BA) 24/32), and superomedial prefrontal cortices (BA 6). Also, an exploratory correlation analysis showed that within 22q11DS children reduced activation was associated with behavioural impairment-social difficulties (measured using the Total Difficulties Score from the Strengths and Difficulties Questionnaire [SDQ]) were significantly negatively correlated with brain activity during fear and disgust processing (respectively) in the left precentral gyrus (BA 4) and in the left fusiform gyrus (FG, BA 19), right lingual gyrus (BA 18), and bilateral cerebellum. CONCLUSIONS: Regions involved in face processing, including fusiform-extrastriate cortices, anterior cingulate gyri, and superomedial prefrontal cortices (BA 6), are activated by facial expressions of fearful, disgusted, and neutral expressions in children with 22q11DS but generally to a lesser degree than in controls. Hypoactivation in these regions may partly explain the social impairments of children with 22q11DS. En ligne : http://dx.doi.org/10.1186/1866-1955-7-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=347

Modulation of atypical brain activation during executive functioning in autism: a pharmacological MRI study of tianeptine / R. H. WICHERS in Molecular Autism, 12 (2021)  

Public ISBD [article]  inMolecular Autism > 12 (2021) . - 14 p. Titre : Modulation of atypical brain activation during executive functioning in autism: a pharmacological MRI study of tianeptine Type de document : Texte imprimé et/ou numérique Auteurs : R. H. WICHERS, Auteur ; J. L. FINDON, Auteur ; A. JELSMA, Auteur ; V. GIAMPIETRO, Auteur ; V. STOENCHEVA, Auteur ; D. M. ROBERTSON, Auteur ; C. M. MURPHY, Auteur ; S. BLAINEY, Auteur ; G. MCALONAN, Auteur ; C. ECKER, Auteur ; K. RUBIA, Auteur ; D. G. M. MURPHY, Auteur ; Eileen DALY, Auteur Article en page(s) : 14 p. Langues : Anglais (eng) Mots-clés : Adult  Antidepressive Agents, Tricyclic/therapeutic use  Attention/drug effects  Autistic Disorder/diagnostic imaging/drug therapy/physiopathology/psychology  Brain/diagnostic imaging/physiopathology  Cross-Over Studies  Double-Blind Method  Executive Function/drug effects  Humans  Magnetic Resonance Imaging  Male  Middle Aged  Pilot Projects  Thiazepines/therapeutic use  Young Adult  Autism spectrum disorder  Executive functioning  Serotonin  Tianeptine  fMRI  grants from Lilly and Shire. The other authors declare that they have no competing  interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is associated with deficits in executive functioning (EF), and these have been suggested to contribute to core as well as co-occurring psychiatric symptoms. The biological basis of these deficits is unknown but may include the serotonergic system, which is involved both in regulating EF in neurotypical populations and in the pathophysiology of ASD. We previously demonstrated that reducing serotonin by acute tryptophan depletion (ATD) shifts differences in brain function during performance of EF tasks towards control levels. However, ATD cannot be easily used in the clinic, and we therefore need to adopt alternative approaches to challenge the serotonin system. Hence, we investigated the role of the serotonergic modulator tianeptine on EF networks in ASD. METHOD: We conducted a pharmacological magnetic resonance imaging study, using a randomized double-blind crossover design, to compare the effect of an acute dosage of 12.5 mg tianeptine and placebo on brain activation during two EF tasks (of response inhibition and sustained attention) in 38 adult males: 19 with ASD and 19 matched controls. RESULTS: Under placebo, compared to controls, individuals with ASD had atypical brain activation in response inhibition regions including the inferior frontal cortex, premotor regions and cerebellum. During sustained attention, individuals with ASD had decreased brain activation in the right middle temporal cortex, right cuneus and left precuneus. Most of the case-control differences in brain function observed under placebo conditions were abolished by tianeptine administration. Also, within ASD individuals, brain functional differences were shifted significantly towards control levels during response inhibition in the inferior frontal and premotor cortices. LIMITATIONS: We conducted a pilot study using a single dose of tianeptine, and therefore, we cannot comment on long-term outcome. CONCLUSIONS: Our findings provide the first evidence that tianeptine can shift atypical brain activation during EF in adults with ASD towards control levels. Future studies should investigate whether this shift in the biology of ASD is maintained after prolonged treatment with tianeptine and whether it improves clinical symptoms. En ligne : http://dx.doi.org/10.1186/s13229-021-00422-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459 [article] Modulation of atypical brain activation during executive functioning in autism: a pharmacological MRI study of tianeptine [Texte imprimé et/ou numérique] / R. H. WICHERS, Auteur ; J. L. FINDON, Auteur ; A. JELSMA, Auteur ; V. GIAMPIETRO, Auteur ; V. STOENCHEVA, Auteur ; D. M. ROBERTSON, Auteur ; C. M. MURPHY, Auteur ; S. BLAINEY, Auteur ; G. MCALONAN, Auteur ; C. ECKER, Auteur ; K. RUBIA, Auteur ; D. G. M. MURPHY, Auteur ; Eileen DALY, Auteur . - 14 p. Langues : Anglais (eng) in Molecular Autism > 12 (2021) . - 14 p. Mots-clés : Adult  Antidepressive Agents, Tricyclic/therapeutic use  Attention/drug effects  Autistic Disorder/diagnostic imaging/drug therapy/physiopathology/psychology  Brain/diagnostic imaging/physiopathology  Cross-Over Studies  Double-Blind Method  Executive Function/drug effects  Humans  Magnetic Resonance Imaging  Male  Middle Aged  Pilot Projects  Thiazepines/therapeutic use  Young Adult  Autism spectrum disorder  Executive functioning  Serotonin  Tianeptine  fMRI  grants from Lilly and Shire. The other authors declare that they have no competing  interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is associated with deficits in executive functioning (EF), and these have been suggested to contribute to core as well as co-occurring psychiatric symptoms. The biological basis of these deficits is unknown but may include the serotonergic system, which is involved both in regulating EF in neurotypical populations and in the pathophysiology of ASD. We previously demonstrated that reducing serotonin by acute tryptophan depletion (ATD) shifts differences in brain function during performance of EF tasks towards control levels. However, ATD cannot be easily used in the clinic, and we therefore need to adopt alternative approaches to challenge the serotonin system. Hence, we investigated the role of the serotonergic modulator tianeptine on EF networks in ASD. METHOD: We conducted a pharmacological magnetic resonance imaging study, using a randomized double-blind crossover design, to compare the effect of an acute dosage of 12.5 mg tianeptine and placebo on brain activation during two EF tasks (of response inhibition and sustained attention) in 38 adult males: 19 with ASD and 19 matched controls. RESULTS: Under placebo, compared to controls, individuals with ASD had atypical brain activation in response inhibition regions including the inferior frontal cortex, premotor regions and cerebellum. During sustained attention, individuals with ASD had decreased brain activation in the right middle temporal cortex, right cuneus and left precuneus. Most of the case-control differences in brain function observed under placebo conditions were abolished by tianeptine administration. Also, within ASD individuals, brain functional differences were shifted significantly towards control levels during response inhibition in the inferior frontal and premotor cortices. LIMITATIONS: We conducted a pilot study using a single dose of tianeptine, and therefore, we cannot comment on long-term outcome. CONCLUSIONS: Our findings provide the first evidence that tianeptine can shift atypical brain activation during EF in adults with ASD towards control levels. Future studies should investigate whether this shift in the biology of ASD is maintained after prolonged treatment with tianeptine and whether it improves clinical symptoms. En ligne : http://dx.doi.org/10.1186/s13229-021-00422-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459

Visuospatial working memory in children and adolescents with 22q11.2 deletion syndrome; an fMRI study / R. AZUMA in Journal of Neurodevelopmental Disorders, 1-1 (March 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-1 (March 2009) . - p.46-60 Titre : Visuospatial working memory in children and adolescents with 22q11.2 deletion syndrome; an fMRI study Type de document : Texte imprimé et/ou numérique Auteurs : R. AZUMA, Auteur ; Eileen DALY, Auteur ; Linda E. CAMPBELL, Auteur ; A. F. STEVENS, Auteur ; Quinton DEELEY, Auteur ; V. GIAMPIETRO, Auteur ; Michael BRAMMER, Auteur ; B. GLASER, Auteur ; F. Z. AMBERY, Auteur ; R. G. MORRIS, Auteur ; S. C. WILLIAMS, Auteur ; M. J. OWEN, Auteur ; D. G. MURPHY, Auteur ; K. C. MURPHY, Auteur Article en page(s) : p.46-60 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : 22q11.2 deletion syndrome (22q11DS) is a genetic disorder associated with a microdeletion of chromosome 22q11. In addition to high rates of neuropsychiatric disorders such as schizophrenia and attention deficit hyperactivity disorder, children with 22q11DS have a specific neuropsychological profile with particular deficits in visuospatial and working memory. However, the neurobiological substrate underlying these deficits is poorly understood. We investigated brain function during a visuospatial working memory (SWM) task in eight children with 22q11DS and 13 healthy controls, using fMRI. Both groups showed task-related activation in dorsolateral prefrontal cortex (DLPFC) and bilateral parietal association cortices. Controls activated parietal and occipital regions significantly more than those with 22q11DS but there was no significant between-group difference in DLPFC. In addition, while controls had a significant age-related increase in the activation of posterior brain regions and an age-related decrease in anterior regions, the 22q11DS children showed the opposite pattern. Genetically determined differences in the development of specific brain systems may underpin the cognitive deficits in 22q11DS, and may contribute to the later development of neuropsychiatric disorders. En ligne : http://dx.doi.org/10.1007/s11689-009-9008-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Visuospatial working memory in children and adolescents with 22q11.2 deletion syndrome; an fMRI study [Texte imprimé et/ou numérique] / R. AZUMA, Auteur ; Eileen DALY, Auteur ; Linda E. CAMPBELL, Auteur ; A. F. STEVENS, Auteur ; Quinton DEELEY, Auteur ; V. GIAMPIETRO, Auteur ; Michael BRAMMER, Auteur ; B. GLASER, Auteur ; F. Z. AMBERY, Auteur ; R. G. MORRIS, Auteur ; S. C. WILLIAMS, Auteur ; M. J. OWEN, Auteur ; D. G. MURPHY, Auteur ; K. C. MURPHY, Auteur . - p.46-60. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-1 (March 2009) . - p.46-60 Index. décimale : PER Périodiques Résumé : 22q11.2 deletion syndrome (22q11DS) is a genetic disorder associated with a microdeletion of chromosome 22q11. In addition to high rates of neuropsychiatric disorders such as schizophrenia and attention deficit hyperactivity disorder, children with 22q11DS have a specific neuropsychological profile with particular deficits in visuospatial and working memory. However, the neurobiological substrate underlying these deficits is poorly understood. We investigated brain function during a visuospatial working memory (SWM) task in eight children with 22q11DS and 13 healthy controls, using fMRI. Both groups showed task-related activation in dorsolateral prefrontal cortex (DLPFC) and bilateral parietal association cortices. Controls activated parietal and occipital regions significantly more than those with 22q11DS but there was no significant between-group difference in DLPFC. In addition, while controls had a significant age-related increase in the activation of posterior brain regions and an age-related decrease in anterior regions, the 22q11DS children showed the opposite pattern. Genetically determined differences in the development of specific brain systems may underpin the cognitive deficits in 22q11DS, and may contribute to the later development of neuropsychiatric disorders. En ligne : http://dx.doi.org/10.1007/s11689-009-9008-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

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