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Developmental phenotype in Phelan-McDermid (22q13.3 deletion) syndrome: a systematic and prospective study in 34 children / R. J. ZWANENBURG in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)
[article]
Titre : Developmental phenotype in Phelan-McDermid (22q13.3 deletion) syndrome: a systematic and prospective study in 34 children Type de document : Texte imprimé et/ou numérique Auteurs : R. J. ZWANENBURG, Auteur ; S. A. RUITER, Auteur ; E. R. VAN DEN HEUVEL, Auteur ; B. C. FLAPPER, Auteur ; C. M. VAN RAVENSWAAIJ-ARTS, Auteur Article en page(s) : p.16 Langues : Anglais (eng) Mots-clés : 22q13 deletion syndrome Autism Developmental phenotype Intellectual disability Neurodevelopmental disorders Phelan-McDermid syndrome Shank3 Index. décimale : PER Périodiques Résumé : BACKGROUND: Phelan-McDermid syndrome (PMS) or 22q13.3 deletion syndrome is characterized by global developmental delay, cognitive deficits, and behaviour in the autism spectrum. Knowledge about developmental and behavioural characteristics of this rare chromosomal disorder is still limited despite a rapid growing number of diagnoses. Our aim was to study a new and relatively large cohort to further characterize the developmental phenotype of children with PMS. METHODS: We performed a descriptive study of children with a 22q13.3 deletion including SHANK3, aged 8 to 178 months, who were systematically (n = 34) and longitudinally (n = 29) assessed with standardized instruments: Bayley Scales of Infant and Toddler Development, third edition; Wechsler Preschool and Primary Scale of Intelligence, third edition; and Vineland Screener for Social and Adaptive Behavior. RESULTS: Maximal developmental functioning ranged from 34 to 52 months depending on the developmental domain. In general, children performed poorest in the domain of language and best on the domain of motor (young children) or cognitive development (older children). At the individual level, 25 % scored better for receptive and 18 % for expressive language, whereas 22 % scored better for fine and 33 % for gross motor function. Developmental quotients were higher in younger children and decreased with age for all developmental domains, with 38 % of the children showing no improvement of cognitive developmental functioning. Almost all children (33/34) had significant deficits in adaptive behaviour. Children with very small deletions, covering only the SHANK3, ACR, and RABL2B genes, had a more favourable developmental phenotype. CONCLUSIONS: Cognitive, motor, and especially language development were significantly impaired in all children with PMS but also highly variable and unpredictable. In addition, deficits in adaptive behaviour further hampered their cognitive development. Therefore, cognitive and behavioural characteristics should be evaluated and followed in each child with PMS to adapt supportive and therapeutic strategies to individual needs. Further research evaluating the relationship between deletion characteristics and the developmental phenotype is warranted to improve counselling of parents. En ligne : http://dx.doi.org/10.1186/s11689-016-9150-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.16[article] Developmental phenotype in Phelan-McDermid (22q13.3 deletion) syndrome: a systematic and prospective study in 34 children [Texte imprimé et/ou numérique] / R. J. ZWANENBURG, Auteur ; S. A. RUITER, Auteur ; E. R. VAN DEN HEUVEL, Auteur ; B. C. FLAPPER, Auteur ; C. M. VAN RAVENSWAAIJ-ARTS, Auteur . - p.16.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.16
Mots-clés : 22q13 deletion syndrome Autism Developmental phenotype Intellectual disability Neurodevelopmental disorders Phelan-McDermid syndrome Shank3 Index. décimale : PER Périodiques Résumé : BACKGROUND: Phelan-McDermid syndrome (PMS) or 22q13.3 deletion syndrome is characterized by global developmental delay, cognitive deficits, and behaviour in the autism spectrum. Knowledge about developmental and behavioural characteristics of this rare chromosomal disorder is still limited despite a rapid growing number of diagnoses. Our aim was to study a new and relatively large cohort to further characterize the developmental phenotype of children with PMS. METHODS: We performed a descriptive study of children with a 22q13.3 deletion including SHANK3, aged 8 to 178 months, who were systematically (n = 34) and longitudinally (n = 29) assessed with standardized instruments: Bayley Scales of Infant and Toddler Development, third edition; Wechsler Preschool and Primary Scale of Intelligence, third edition; and Vineland Screener for Social and Adaptive Behavior. RESULTS: Maximal developmental functioning ranged from 34 to 52 months depending on the developmental domain. In general, children performed poorest in the domain of language and best on the domain of motor (young children) or cognitive development (older children). At the individual level, 25 % scored better for receptive and 18 % for expressive language, whereas 22 % scored better for fine and 33 % for gross motor function. Developmental quotients were higher in younger children and decreased with age for all developmental domains, with 38 % of the children showing no improvement of cognitive developmental functioning. Almost all children (33/34) had significant deficits in adaptive behaviour. Children with very small deletions, covering only the SHANK3, ACR, and RABL2B genes, had a more favourable developmental phenotype. CONCLUSIONS: Cognitive, motor, and especially language development were significantly impaired in all children with PMS but also highly variable and unpredictable. In addition, deficits in adaptive behaviour further hampered their cognitive development. Therefore, cognitive and behavioural characteristics should be evaluated and followed in each child with PMS to adapt supportive and therapeutic strategies to individual needs. Further research evaluating the relationship between deletion characteristics and the developmental phenotype is warranted to improve counselling of parents. En ligne : http://dx.doi.org/10.1186/s11689-016-9150-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348 Emotion regulation and development in children with autism and 22q13 Deletion Syndrome: Evidence for group differences / Sarah E. GLASER in Research in Autism Spectrum Disorders, 5-2 (April-June 2011)
[article]
Titre : Emotion regulation and development in children with autism and 22q13 Deletion Syndrome: Evidence for group differences Type de document : Texte imprimé et/ou numérique Auteurs : Sarah E. GLASER, Auteur ; Steven R. SHAW, Auteur Année de publication : 2011 Article en page(s) : p.926-934 Langues : Anglais (eng) Mots-clés : Autism 22q13 Deletion Syndrome Emotion regulation Social–emotional development Intellectual disabilities Index. décimale : PER Périodiques Résumé : Emotion regulation (ER) abilities and developmental differences were investigated among 19 children with autism and 18 children with 22q13 Deletion Syndrome (a rare chromosomal disorder with certain autistic symptoms). The purpose of this study was to examine the phenotypic similarities between the two disorders. ER was measured by the Temperament and Atypical Behavior Scale (TABS) and development was measured by the Developmental Profile – Third Edition (DP-3). It was hypothesized that children with autism would score higher on the Detached domain of the TABS because the domain is associated with autism spectrum disorders. It was also hypothesized that because of similarly well established cognitive and communicative deficits between the two populations, no significant differences in development would be found. Results indicated that the autism group was significantly more impaired on the Detached domain of the TABS and scored higher on every domain of the DP-3 except in social–emotional skills. These findings differentiate the phenotypes of the two disorders and suggest that detached emotional behavior is more salient among children with autism. Early intervention programs that target the improvement of ER and social skills may ensure healthier behavioral outcomes for these individuals. En ligne : http://dx.doi.org/10.1016/j.rasd.2010.11.001 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=114
in Research in Autism Spectrum Disorders > 5-2 (April-June 2011) . - p.926-934[article] Emotion regulation and development in children with autism and 22q13 Deletion Syndrome: Evidence for group differences [Texte imprimé et/ou numérique] / Sarah E. GLASER, Auteur ; Steven R. SHAW, Auteur . - 2011 . - p.926-934.
Langues : Anglais (eng)
in Research in Autism Spectrum Disorders > 5-2 (April-June 2011) . - p.926-934
Mots-clés : Autism 22q13 Deletion Syndrome Emotion regulation Social–emotional development Intellectual disabilities Index. décimale : PER Périodiques Résumé : Emotion regulation (ER) abilities and developmental differences were investigated among 19 children with autism and 18 children with 22q13 Deletion Syndrome (a rare chromosomal disorder with certain autistic symptoms). The purpose of this study was to examine the phenotypic similarities between the two disorders. ER was measured by the Temperament and Atypical Behavior Scale (TABS) and development was measured by the Developmental Profile – Third Edition (DP-3). It was hypothesized that children with autism would score higher on the Detached domain of the TABS because the domain is associated with autism spectrum disorders. It was also hypothesized that because of similarly well established cognitive and communicative deficits between the two populations, no significant differences in development would be found. Results indicated that the autism group was significantly more impaired on the Detached domain of the TABS and scored higher on every domain of the DP-3 except in social–emotional skills. These findings differentiate the phenotypes of the two disorders and suggest that detached emotional behavior is more salient among children with autism. Early intervention programs that target the improvement of ER and social skills may ensure healthier behavioral outcomes for these individuals. En ligne : http://dx.doi.org/10.1016/j.rasd.2010.11.001 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=114 Phelan-McDermid syndrome: a review of the literature and practice parameters for medical assessment and monitoring / A. KOLEVZON in Journal of Neurodevelopmental Disorders, 6-1 (December 2014)
[article]
Titre : Phelan-McDermid syndrome: a review of the literature and practice parameters for medical assessment and monitoring Type de document : Texte imprimé et/ou numérique Auteurs : A. KOLEVZON, Auteur ; Benjamin ANGARITA, Auteur ; L. BUSH, Auteur ; A. Ting WANG, Auteur ; Y. FRANK, Auteur ; A. YANG, Auteur ; R. RAPAPORT, Auteur ; J. SALAND, Auteur ; S. SRIVASTAVA, Auteur ; C. FARRELL, Auteur ; L. J. EDELMANN, Auteur ; Joseph D. BUXBAUM, Auteur Article en page(s) : p.39 Langues : Anglais (eng) Mots-clés : 22q13 deletion syndrome Autism Autism spectrum disorder Neurodevelopmental disorders Phelan-McDermid syndrome Practice parameters Shank3 Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) and intellectual disability (ID) can be caused by mutations in a large number of genes. One example is SHANK3 on the terminal end of chromosome 22q. Loss of one functional copy of SHANK3 results in 22q13 deletion syndrome or Phelan-McDermid syndrome (PMS) and causes a monogenic form of ASD and/or ID with a frequency of 0.5% to 2% of cases. SHANK3 is the critical gene in this syndrome, and its loss results in disruption of synaptic function. With chromosomal microarray analyses now a standard of care in the assessment of ASD and developmental delay, and with the emergence of whole exome and whole genome sequencing in this context, identification of PMS in routine clinical settings will increase significantly. However, PMS remains a rare disorder, and the majority of physicians have never seen a case. While there is agreement about core deficits of PMS, there have been no established parameters to guide evaluation and medical monitoring of the syndrome. Evaluations must include a thorough history and physical and dysmorphology examination. Neurological deficits, including the presence of seizures and structural brain abnormalities should be assessed as well as motor deficits. Endocrine, renal, cardiac, and gastrointestinal problems all require assessment and monitoring in addition to the risk of recurring infections, dental and vision problems, and lymphedema. Finally, all patients should have cognitive, behavioral, and ASD evaluations. The objective of this paper is to address this gap in the literature and establish recommendations to assess the medical, genetic, and neurological features of PMS. En ligne : http://dx.doi.org/10.1186/1866-1955-6-39 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=347
in Journal of Neurodevelopmental Disorders > 6-1 (December 2014) . - p.39[article] Phelan-McDermid syndrome: a review of the literature and practice parameters for medical assessment and monitoring [Texte imprimé et/ou numérique] / A. KOLEVZON, Auteur ; Benjamin ANGARITA, Auteur ; L. BUSH, Auteur ; A. Ting WANG, Auteur ; Y. FRANK, Auteur ; A. YANG, Auteur ; R. RAPAPORT, Auteur ; J. SALAND, Auteur ; S. SRIVASTAVA, Auteur ; C. FARRELL, Auteur ; L. J. EDELMANN, Auteur ; Joseph D. BUXBAUM, Auteur . - p.39.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 6-1 (December 2014) . - p.39
Mots-clés : 22q13 deletion syndrome Autism Autism spectrum disorder Neurodevelopmental disorders Phelan-McDermid syndrome Practice parameters Shank3 Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) and intellectual disability (ID) can be caused by mutations in a large number of genes. One example is SHANK3 on the terminal end of chromosome 22q. Loss of one functional copy of SHANK3 results in 22q13 deletion syndrome or Phelan-McDermid syndrome (PMS) and causes a monogenic form of ASD and/or ID with a frequency of 0.5% to 2% of cases. SHANK3 is the critical gene in this syndrome, and its loss results in disruption of synaptic function. With chromosomal microarray analyses now a standard of care in the assessment of ASD and developmental delay, and with the emergence of whole exome and whole genome sequencing in this context, identification of PMS in routine clinical settings will increase significantly. However, PMS remains a rare disorder, and the majority of physicians have never seen a case. While there is agreement about core deficits of PMS, there have been no established parameters to guide evaluation and medical monitoring of the syndrome. Evaluations must include a thorough history and physical and dysmorphology examination. Neurological deficits, including the presence of seizures and structural brain abnormalities should be assessed as well as motor deficits. Endocrine, renal, cardiac, and gastrointestinal problems all require assessment and monitoring in addition to the risk of recurring infections, dental and vision problems, and lymphedema. Finally, all patients should have cognitive, behavioral, and ASD evaluations. The objective of this paper is to address this gap in the literature and establish recommendations to assess the medical, genetic, and neurological features of PMS. En ligne : http://dx.doi.org/10.1186/1866-1955-6-39 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=347 Brief Report: Sensory Reactivity in Children with Phelan–McDermid Syndrome / A. M. MIESES in Journal of Autism and Developmental Disorders, 46-7 (July 2016)
[article]
Titre : Brief Report: Sensory Reactivity in Children with Phelan–McDermid Syndrome Type de document : Texte imprimé et/ou numérique Auteurs : A. M. MIESES, Auteur ; Teresa TAVASSOLI, Auteur ; E. LI, Auteur ; L. SOORYA, Auteur ; S. LURIE, Auteur ; A. Ting WANG, Auteur ; P. M. SIPER, Auteur ; A. KOLEVZON, Auteur Article en page(s) : p.2508-2513 Langues : Anglais (eng) Mots-clés : Phelan–McDermid syndrome 22q13 deletion syndrome Autism Autism spectrum disorder Sensory reactivity Sensory profile Index. décimale : PER Périodiques Résumé : Phelan–McDermid syndrome (PMS), a monogenic form of autism spectrum disorder (ASD), results from deletion or mutation of the SHANK3 gene. Atypical sensory reactivity is now included in the diagnostic criteria for ASD. Examining the sensory phenotype in monogenic forms of ASD, such as PMS, may help identify underlying mechanisms of sensory reactivity. Using the Short Sensory Profile, the current study compared sensory reactivity in 24 children with PMS to 61 children with idiopathic ASD (iASD). Results suggest that children with PMS show more low energy/weak symptoms and less sensory sensitivity as compared to children with iASD. This study is the first to demonstrate differences in sensory reactivity between children with PMS and iASD, helping to refine the PMS phenotype. En ligne : http://dx.doi.org/10.1007/s10803-016-2754-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=290
in Journal of Autism and Developmental Disorders > 46-7 (July 2016) . - p.2508-2513[article] Brief Report: Sensory Reactivity in Children with Phelan–McDermid Syndrome [Texte imprimé et/ou numérique] / A. M. MIESES, Auteur ; Teresa TAVASSOLI, Auteur ; E. LI, Auteur ; L. SOORYA, Auteur ; S. LURIE, Auteur ; A. Ting WANG, Auteur ; P. M. SIPER, Auteur ; A. KOLEVZON, Auteur . - p.2508-2513.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 46-7 (July 2016) . - p.2508-2513
Mots-clés : Phelan–McDermid syndrome 22q13 deletion syndrome Autism Autism spectrum disorder Sensory reactivity Sensory profile Index. décimale : PER Périodiques Résumé : Phelan–McDermid syndrome (PMS), a monogenic form of autism spectrum disorder (ASD), results from deletion or mutation of the SHANK3 gene. Atypical sensory reactivity is now included in the diagnostic criteria for ASD. Examining the sensory phenotype in monogenic forms of ASD, such as PMS, may help identify underlying mechanisms of sensory reactivity. Using the Short Sensory Profile, the current study compared sensory reactivity in 24 children with PMS to 61 children with idiopathic ASD (iASD). Results suggest that children with PMS show more low energy/weak symptoms and less sensory sensitivity as compared to children with iASD. This study is the first to demonstrate differences in sensory reactivity between children with PMS and iASD, helping to refine the PMS phenotype. En ligne : http://dx.doi.org/10.1007/s10803-016-2754-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=290 Delineation of the genetic and clinical spectrum of Phelan-McDermid syndrome caused by SHANK3 point mutations / S. DE RUBEIS in Molecular Autism, 9 (2018)
[article]
Titre : Delineation of the genetic and clinical spectrum of Phelan-McDermid syndrome caused by SHANK3 point mutations Type de document : Texte imprimé et/ou numérique Auteurs : S. DE RUBEIS, Auteur ; P. M. SIPER, Auteur ; A. DURKIN, Auteur ; J. WEISSMAN, Auteur ; F. MURATET, Auteur ; Danielle B. HALPERN, Auteur ; M. D. P. TRELLES, Auteur ; Y. FRANK, Auteur ; R. LOZANO, Auteur ; A. Ting WANG, Auteur ; J. L. HOLDER, Auteur ; Catalina BETANCUR, Auteur ; Joseph D. BUXBAUM, Auteur ; A. KOLEVZON, Auteur Article en page(s) : 31p. Langues : Anglais (eng) Mots-clés : Adolescent Adult Child Child, Preschool Chromosome Deletion Chromosome Disorders/genetics/pathology Chromosomes, Human, Pair 22/genetics Female Haploinsufficiency Humans Male Nerve Tissue Proteins/genetics Phenotype Point Mutation 22q13 deletion syndrome Autism spectrum disorder Intellectual disability Phelan-McDermid syndrome shank3 Sequence variants Index. décimale : PER Périodiques Résumé : Background: Phelan-McDermid syndrome (PMS) is a neurodevelopmental disorder characterized by psychiatric and neurological features. Most reported cases are caused by 22q13.3 deletions, leading to SHANK3 haploinsufficiency, but also usually encompassing many other genes. While the number of point mutations identified in SHANK3 has increased in recent years due to large-scale sequencing studies, systematic studies describing the phenotype of individuals harboring such mutations are lacking. Methods: We provide detailed clinical and genetic data on 17 individuals carrying mutations in SHANK3. We also review 60 previously reported patients with pathogenic or likely pathogenic SHANK3 variants, often lacking detailed phenotypic information. Results: SHANK3 mutations in our cohort and in previously reported cases were distributed throughout the protein; the majority were truncating and all were compatible with de novo inheritance. Despite substantial allelic heterogeneity, four variants were recurrent (p.Leu1142Valfs*153, p.Ala1227Glyfs*69, p.Arg1255Leufs*25, and c.2265+1G>A), suggesting that these are hotspots for de novo mutations. All individuals studied had intellectual disability, and autism spectrum disorder was prevalent (73%). Severe speech deficits were common, but in contrast to individuals with 22q13.3 deletions, the majority developed single words, including 41% with at least phrase speech. Other common findings were consistent with reports among individuals with 22q13.3 deletions, including hypotonia, motor skill deficits, regression, seizures, brain abnormalities, mild dysmorphic features, and feeding and gastrointestinal problems. Conclusions: Haploinsufficiency of SHANK3 resulting from point mutations is sufficient to cause a broad range of features associated with PMS. Our findings expand the molecular and phenotypic spectrum of PMS caused by SHANK3 point mutations and suggest that, in general, speech impairment and motor deficits are more severe in the case of deletions. In contrast, renal abnormalities associated with 22q13.3 deletions do not appear to be related to the loss of SHANK3. En ligne : https://dx.doi.org/10.1186/s13229-018-0205-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371
in Molecular Autism > 9 (2018) . - 31p.[article] Delineation of the genetic and clinical spectrum of Phelan-McDermid syndrome caused by SHANK3 point mutations [Texte imprimé et/ou numérique] / S. DE RUBEIS, Auteur ; P. M. SIPER, Auteur ; A. DURKIN, Auteur ; J. WEISSMAN, Auteur ; F. MURATET, Auteur ; Danielle B. HALPERN, Auteur ; M. D. P. TRELLES, Auteur ; Y. FRANK, Auteur ; R. LOZANO, Auteur ; A. Ting WANG, Auteur ; J. L. HOLDER, Auteur ; Catalina BETANCUR, Auteur ; Joseph D. BUXBAUM, Auteur ; A. KOLEVZON, Auteur . - 31p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 31p.
Mots-clés : Adolescent Adult Child Child, Preschool Chromosome Deletion Chromosome Disorders/genetics/pathology Chromosomes, Human, Pair 22/genetics Female Haploinsufficiency Humans Male Nerve Tissue Proteins/genetics Phenotype Point Mutation 22q13 deletion syndrome Autism spectrum disorder Intellectual disability Phelan-McDermid syndrome shank3 Sequence variants Index. décimale : PER Périodiques Résumé : Background: Phelan-McDermid syndrome (PMS) is a neurodevelopmental disorder characterized by psychiatric and neurological features. Most reported cases are caused by 22q13.3 deletions, leading to SHANK3 haploinsufficiency, but also usually encompassing many other genes. While the number of point mutations identified in SHANK3 has increased in recent years due to large-scale sequencing studies, systematic studies describing the phenotype of individuals harboring such mutations are lacking. Methods: We provide detailed clinical and genetic data on 17 individuals carrying mutations in SHANK3. We also review 60 previously reported patients with pathogenic or likely pathogenic SHANK3 variants, often lacking detailed phenotypic information. Results: SHANK3 mutations in our cohort and in previously reported cases were distributed throughout the protein; the majority were truncating and all were compatible with de novo inheritance. Despite substantial allelic heterogeneity, four variants were recurrent (p.Leu1142Valfs*153, p.Ala1227Glyfs*69, p.Arg1255Leufs*25, and c.2265+1G>A), suggesting that these are hotspots for de novo mutations. All individuals studied had intellectual disability, and autism spectrum disorder was prevalent (73%). Severe speech deficits were common, but in contrast to individuals with 22q13.3 deletions, the majority developed single words, including 41% with at least phrase speech. Other common findings were consistent with reports among individuals with 22q13.3 deletions, including hypotonia, motor skill deficits, regression, seizures, brain abnormalities, mild dysmorphic features, and feeding and gastrointestinal problems. Conclusions: Haploinsufficiency of SHANK3 resulting from point mutations is sufficient to cause a broad range of features associated with PMS. Our findings expand the molecular and phenotypic spectrum of PMS caused by SHANK3 point mutations and suggest that, in general, speech impairment and motor deficits are more severe in the case of deletions. In contrast, renal abnormalities associated with 22q13.3 deletions do not appear to be related to the loss of SHANK3. En ligne : https://dx.doi.org/10.1186/s13229-018-0205-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371 Neuropsychiatric decompensation in adolescents and adults with Phelan-McDermid syndrome: a systematic review of the literature / A. KOLEVZON in Molecular Autism, 10 (2019)
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PermalinkLanguage ENvironment Analysis (LENA) in Phelan-McDermid Syndrome: Validity and Suggestions for Use in Minimally Verbal Children with Autism Spectrum Disorder / Jacquelin RANKINE in Journal of Autism and Developmental Disorders, 47-6 (June 2017)
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