- <Centre d'Information et de documentation du CRA Rhône-Alpes
- CRA
- Informations pratiques
-
Adresse
Centre d'information et de documentation
Horaires
du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexLundi au Vendredi
Contact
9h00-12h00 13h30-16h00Tél: +33(0)4 37 91 54 65
Mail
Fax: +33(0)4 37 91 54 37
-
Adresse
Détail de l'auteur
Auteur Charlotte E. BLACKMORE |
Documents disponibles écrits par cet auteur (2)
Faire une suggestion Affiner la recherche
Adults with autism spectrum disorder and the criminal justice system: An investigation of prevalence of contact with the criminal justice system, risk factors and sex differences in a specialist assessment service / Charlotte E. BLACKMORE in Autism, 26-8 (November 2022)
[article]
Titre : Adults with autism spectrum disorder and the criminal justice system: An investigation of prevalence of contact with the criminal justice system, risk factors and sex differences in a specialist assessment service Type de document : Texte imprimé et/ou numérique Auteurs : Charlotte E. BLACKMORE, Auteur ; Emma L. WOODHOUSE, Auteur ; Nicola GILLAN, Auteur ; Ellie WILSON, Auteur ; Karen L. ASHWOOD, Auteur ; Vladimira STOENCHEVA, Auteur ; Alexandra NOLAN, Auteur ; Gráinne M. MCALONAN, Auteur ; Dene M. ROBERTSON, Auteur ; Susannah WHITWELL, Auteur ; Quinton DEELEY, Auteur ; Michael C. CRAIG, Auteur ; Janneke ZINKSTOK, Auteur ; Rob WICHERS, Auteur ; Debbie SPAIN, Auteur ; Ged ROBERTS, Auteur ; Declan GM MURPHY, Auteur ; Clodagh M. MURPHY, Auteur ; Eileen DALY, Auteur Article en page(s) : p.2098-2107 Langues : Anglais (eng) Mots-clés : Adult Humans Male Female Autism Spectrum Disorder/epidemiology Criminal Law Prevalence Sex Characteristics Risk Factors autism spectrum disorders crime criminal justice system offending risk factors research, authorship and/or publication of this article. Index. décimale : PER Périodiques Résumé : There has been growing interest in offending and contact with the criminal justice system (CJS) by people with autism spectrum disorder (ASD). However, it is not clear whether people with ASD offend more than those without ASD. Studies have started to look at whether there are particular offences people with ASD are more likely to commit and whether there are any factors that can affect whether someone comes into contact with the CJS as a potential suspect. This study looked at the patients who attended an ASD diagnostic service over a 17-year period to see the rate of contact with the CJS of those who were diagnosed with ASD and whether there were any particular factors that might increase the risk of CJS contact. Nearly a quarter of the ASD group had some contact with the CJS as a potential suspect. Factors that seemed to increase whether someone with ASD was more likely to have contact with the CJS were being male, being diagnosed with ADHD, and being diagnosed with psychosis. This study is one of the largest studies to investigate the rate of CJS contact as a potential suspect in a sample of adults with ASD in an attempt to give a clearer picture of what might influence someone with ASD to engage in offending behaviour in order to try to see what mental health services can offer to reduce the likelihood of someone with ASD coming into contact with the CJS, for example, treatment for another condition or support. En ligne : http://dx.doi.org/10.1177/13623613221081343 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=488
in Autism > 26-8 (November 2022) . - p.2098-2107[article] Adults with autism spectrum disorder and the criminal justice system: An investigation of prevalence of contact with the criminal justice system, risk factors and sex differences in a specialist assessment service [Texte imprimé et/ou numérique] / Charlotte E. BLACKMORE, Auteur ; Emma L. WOODHOUSE, Auteur ; Nicola GILLAN, Auteur ; Ellie WILSON, Auteur ; Karen L. ASHWOOD, Auteur ; Vladimira STOENCHEVA, Auteur ; Alexandra NOLAN, Auteur ; Gráinne M. MCALONAN, Auteur ; Dene M. ROBERTSON, Auteur ; Susannah WHITWELL, Auteur ; Quinton DEELEY, Auteur ; Michael C. CRAIG, Auteur ; Janneke ZINKSTOK, Auteur ; Rob WICHERS, Auteur ; Debbie SPAIN, Auteur ; Ged ROBERTS, Auteur ; Declan GM MURPHY, Auteur ; Clodagh M. MURPHY, Auteur ; Eileen DALY, Auteur . - p.2098-2107.
Langues : Anglais (eng)
in Autism > 26-8 (November 2022) . - p.2098-2107
Mots-clés : Adult Humans Male Female Autism Spectrum Disorder/epidemiology Criminal Law Prevalence Sex Characteristics Risk Factors autism spectrum disorders crime criminal justice system offending risk factors research, authorship and/or publication of this article. Index. décimale : PER Périodiques Résumé : There has been growing interest in offending and contact with the criminal justice system (CJS) by people with autism spectrum disorder (ASD). However, it is not clear whether people with ASD offend more than those without ASD. Studies have started to look at whether there are particular offences people with ASD are more likely to commit and whether there are any factors that can affect whether someone comes into contact with the CJS as a potential suspect. This study looked at the patients who attended an ASD diagnostic service over a 17-year period to see the rate of contact with the CJS of those who were diagnosed with ASD and whether there were any particular factors that might increase the risk of CJS contact. Nearly a quarter of the ASD group had some contact with the CJS as a potential suspect. Factors that seemed to increase whether someone with ASD was more likely to have contact with the CJS were being male, being diagnosed with ADHD, and being diagnosed with psychosis. This study is one of the largest studies to investigate the rate of CJS contact as a potential suspect in a sample of adults with ASD in an attempt to give a clearer picture of what might influence someone with ASD to engage in offending behaviour in order to try to see what mental health services can offer to reduce the likelihood of someone with ASD coming into contact with the CJS, for example, treatment for another condition or support. En ligne : http://dx.doi.org/10.1177/13623613221081343 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=488 Neuroanatomical underpinnings of autism symptomatology in carriers and non-carriers of the 22q11.2 microdeletion / Maria GUDBRANDSEN in Molecular Autism, 11 (2020)
[article]
Titre : Neuroanatomical underpinnings of autism symptomatology in carriers and non-carriers of the 22q11.2 microdeletion Type de document : Texte imprimé et/ou numérique Auteurs : Maria GUDBRANDSEN, Auteur ; Anke BLETSCH, Auteur ; Caroline MANN, Auteur ; Eileen DALY, Auteur ; Clodagh M. MURPHY, Auteur ; Vladimira STOENCHEVA, Auteur ; Charlotte E. BLACKMORE, Auteur ; Maria ROGDAKI, Auteur ; Leila KUSHAN, Auteur ; Carrie E. BEARDEN, Auteur ; Declan G. M. MURPHY, Auteur ; Michael C. CRAIG, Auteur ; Christine ECKER, Auteur Article en page(s) : 46 p. Langues : Anglais (eng) Mots-clés : 22q11.2 deletion syndrome Autism spectrum disorder Brain anatomy Neurodevelopment Surface-based anatomy authors reported any financial interests or conflicts of interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: A crucial step to understanding the mechanistic underpinnings of autism spectrum disorder (ASD), is to examine if the biological underpinnings of ASD in genetic high-risk conditions, like 22q11.2 deletion syndrome (22q11.2DS), are similar to those in idiopathic illness. This study aimed to examine if ASD symptomatology in 22q11.2DS is underpinned by the same-or distinct-neural systems that mediate these symptoms in non-deletion carriers. METHODS: We examined vertex-wise estimates of cortical volume (CV), surface area (SA), and cortical thickness across 131 individuals between 6 and 25?years of age including (1) 50 individuals with 22q11.2DS, out of which n = 25 had a diagnosis of ASD, (2) 40 non-carriers of the microdeletion with a diagnosis of ASD (i.e., idiopathic ASD), and (3) 41 typically developing (TD) controls. We employed a 2-by-2 factorial design to identify neuroanatomical variability associated with the main effects of 22q11.2DS and ASD, as well as their interaction. Further, using canonical correlation analysis (CCA), we compared neuroanatomical variability associated with the complex (i.e., multivariate) clinical phenotype of ASD between 22q11.2 deletion carriers and non-carriers. RESULTS: The set of brain regions associated with the main effect of 22q11.2DS was distinct from the neuroanatomical underpinnings of the main effect of ASD. Moreover, significant 22q11.2DS-by-ASD interactions were observed for CV and SA in the dorsolateral prefrontal cortex, precentral gyrus, and posterior cingulate cortex, suggesting that the neuroanatomy of ASD is significantly modulated by 22q11.2DS (p < 0.01). We further established that the multivariate patterns of neuroanatomical variability associated with differences in symptom profiles significantly differed between 22q11.2 deletion carriers and non-carriers. LIMITATIONS: We employed a multicenter design to overcome single-site recruitment limitations; however, FreeSurfer-derived measures of surface anatomy have been shown to be highly reliable across scanner platforms and field strengths. Further, we controlled for gender to address the differing distribution between idiopathic ASD individuals and the other groups. Nonetheless, the gender distribution in our sample reflects that of the respective populations, adding to the generalizability of our results. Last, we included individuals with a relatively wide age range (i.e., 6-25?years). CONCLUSIONS: Our findings indicate that neuroanatomical correlates of ASD symptomatology in carriers of the 22q11.2 microdeletion diverge from those in idiopathic ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00356-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427
in Molecular Autism > 11 (2020) . - 46 p.[article] Neuroanatomical underpinnings of autism symptomatology in carriers and non-carriers of the 22q11.2 microdeletion [Texte imprimé et/ou numérique] / Maria GUDBRANDSEN, Auteur ; Anke BLETSCH, Auteur ; Caroline MANN, Auteur ; Eileen DALY, Auteur ; Clodagh M. MURPHY, Auteur ; Vladimira STOENCHEVA, Auteur ; Charlotte E. BLACKMORE, Auteur ; Maria ROGDAKI, Auteur ; Leila KUSHAN, Auteur ; Carrie E. BEARDEN, Auteur ; Declan G. M. MURPHY, Auteur ; Michael C. CRAIG, Auteur ; Christine ECKER, Auteur . - 46 p.
Langues : Anglais (eng)
in Molecular Autism > 11 (2020) . - 46 p.
Mots-clés : 22q11.2 deletion syndrome Autism spectrum disorder Brain anatomy Neurodevelopment Surface-based anatomy authors reported any financial interests or conflicts of interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: A crucial step to understanding the mechanistic underpinnings of autism spectrum disorder (ASD), is to examine if the biological underpinnings of ASD in genetic high-risk conditions, like 22q11.2 deletion syndrome (22q11.2DS), are similar to those in idiopathic illness. This study aimed to examine if ASD symptomatology in 22q11.2DS is underpinned by the same-or distinct-neural systems that mediate these symptoms in non-deletion carriers. METHODS: We examined vertex-wise estimates of cortical volume (CV), surface area (SA), and cortical thickness across 131 individuals between 6 and 25?years of age including (1) 50 individuals with 22q11.2DS, out of which n = 25 had a diagnosis of ASD, (2) 40 non-carriers of the microdeletion with a diagnosis of ASD (i.e., idiopathic ASD), and (3) 41 typically developing (TD) controls. We employed a 2-by-2 factorial design to identify neuroanatomical variability associated with the main effects of 22q11.2DS and ASD, as well as their interaction. Further, using canonical correlation analysis (CCA), we compared neuroanatomical variability associated with the complex (i.e., multivariate) clinical phenotype of ASD between 22q11.2 deletion carriers and non-carriers. RESULTS: The set of brain regions associated with the main effect of 22q11.2DS was distinct from the neuroanatomical underpinnings of the main effect of ASD. Moreover, significant 22q11.2DS-by-ASD interactions were observed for CV and SA in the dorsolateral prefrontal cortex, precentral gyrus, and posterior cingulate cortex, suggesting that the neuroanatomy of ASD is significantly modulated by 22q11.2DS (p < 0.01). We further established that the multivariate patterns of neuroanatomical variability associated with differences in symptom profiles significantly differed between 22q11.2 deletion carriers and non-carriers. LIMITATIONS: We employed a multicenter design to overcome single-site recruitment limitations; however, FreeSurfer-derived measures of surface anatomy have been shown to be highly reliable across scanner platforms and field strengths. Further, we controlled for gender to address the differing distribution between idiopathic ASD individuals and the other groups. Nonetheless, the gender distribution in our sample reflects that of the respective populations, adding to the generalizability of our results. Last, we included individuals with a relatively wide age range (i.e., 6-25?years). CONCLUSIONS: Our findings indicate that neuroanatomical correlates of ASD symptomatology in carriers of the 22q11.2 microdeletion diverge from those in idiopathic ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00356-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427