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Mention de date : September 2010
Paru le : 01/09/2010 |
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[n° ou bulletin]
2-3 - September 2010 [Texte imprimé et/ou numérique] . - 2010. Langues : Anglais (eng)
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[article]
Titre : Cover essay Type de document : Texte imprimé et/ou numérique Auteurs : J. PIVEN, Auteur Article en page(s) : p.119 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-010-9057-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.119[article] Cover essay [Texte imprimé et/ou numérique] / J. PIVEN, Auteur . - p.119.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.119
Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-010-9057-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 Using animal models of enriched environments to inform research on sensory integration intervention for the rehabilitation of neurodevelopmental disorders / S. REYNOLDS in Journal of Neurodevelopmental Disorders, 2-3 (September 2010)
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[article]
Titre : Using animal models of enriched environments to inform research on sensory integration intervention for the rehabilitation of neurodevelopmental disorders Type de document : Texte imprimé et/ou numérique Auteurs : S. REYNOLDS, Auteur ; S. J. LANE, Auteur ; L. RICHARDS, Auteur Article en page(s) : p.120-32 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The field of behavioral neuroscience has been successful in using an animal model of enriched environments for over five decades to measure the rehabilitative and preventative effects of sensory, cognitive and motor stimulation in animal models. Several key principles of enriched environments match those used in sensory integration therapy, a treatment used for children with neurodevelopmental disorders. This paper reviews the paradigm of environmental enrichment, compares animal models of enriched environments to principles of sensory integration treatment, and discusses applications for the rehabilitation of neurodevelopmental disorders. Based on this review, the essential features in the enriched environment paradigm which should be included in sensory integration treatment are multiple sensory experiences, novelty in the environment, and active engagement in challenging cognitive, sensory, and motor tasks. Use of sensory integration treatment may be most applicable for children with anxiety, hypersensitivity, repetitive behaviors or heightened levels of stress. Additionally, individuals with deficits in social behavior, social participation, or impairments in learning and memory may show gains with this type of treatment. En ligne : http://dx.doi.org/10.1007/s11689-010-9053-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.120-32[article] Using animal models of enriched environments to inform research on sensory integration intervention for the rehabilitation of neurodevelopmental disorders [Texte imprimé et/ou numérique] / S. REYNOLDS, Auteur ; S. J. LANE, Auteur ; L. RICHARDS, Auteur . - p.120-32.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.120-32
Index. décimale : PER Périodiques Résumé : The field of behavioral neuroscience has been successful in using an animal model of enriched environments for over five decades to measure the rehabilitative and preventative effects of sensory, cognitive and motor stimulation in animal models. Several key principles of enriched environments match those used in sensory integration therapy, a treatment used for children with neurodevelopmental disorders. This paper reviews the paradigm of environmental enrichment, compares animal models of enriched environments to principles of sensory integration treatment, and discusses applications for the rehabilitation of neurodevelopmental disorders. Based on this review, the essential features in the enriched environment paradigm which should be included in sensory integration treatment are multiple sensory experiences, novelty in the environment, and active engagement in challenging cognitive, sensory, and motor tasks. Use of sensory integration treatment may be most applicable for children with anxiety, hypersensitivity, repetitive behaviors or heightened levels of stress. Additionally, individuals with deficits in social behavior, social participation, or impairments in learning and memory may show gains with this type of treatment. En ligne : http://dx.doi.org/10.1007/s11689-010-9053-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 Hippocampus specific iron deficiency alters competition and cooperation between developing memory systems / E. S. CARLSON in Journal of Neurodevelopmental Disorders, 2-3 (September 2010)
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[article]
Titre : Hippocampus specific iron deficiency alters competition and cooperation between developing memory systems Type de document : Texte imprimé et/ou numérique Auteurs : E. S. CARLSON, Auteur ; S. J. FRETHAM, Auteur ; E. UNGER, Auteur ; M. O'CONNOR, Auteur ; A. PETRYK, Auteur ; T. SCHALLERT, Auteur ; R. RAO, Auteur ; I. TKAC, Auteur ; Michael K. GEORGIEFF, Auteur Article en page(s) : p.133-43 Langues : Anglais (eng) Mots-clés : DMT1, Slc11a2, Nuclear magnetic resonance spectroscopy Hippocampus Iron deficiency Memory systems Morris water maze Procedural memory Spatial memory Striatum Index. décimale : PER Périodiques Résumé : UNLABELLED: Iron deficiency (ID) is the most common gestational micronutrient deficiency in the world, targets the fetal hippocampus and striatum and results in long-term behavioral abnormalities. These structures primarily mediate spatial and procedural memory, respectively, in the rodent but have interconnections that result in competition or cooperation during cognitive tasks. We determined whether ID-induced impairment of one alters the function of the other by genetically inducing a 40% reduction of hippocampus iron content in late fetal life in mice and measuring dorsal striatal gene expression and metabolism and the behavioral balance between the two memory systems in adulthood. Slc11a2(hipp/hipp) mice had similar striatum iron content, but 18% lower glucose and 44% lower lactate levels, a 30% higher phosphocreatine:creatine ratio, and reduced iron transporter gene expression compared to wild type (WT) littermates, implying reduced striatal metabolic function. Slc11a2(hipp/hipp) mice had longer mean escape times on a cued task paradigm implying impaired procedural memory. Nevertheless, when hippocampal and striatal memory systems were placed in competition using a Morris Water Maze task that alternates spatial navigation and visual cued responses during training, and forces a choice between hippocampal and striatal strategies during probe trials, Slc11a2(hipp/hipp) mice used the hippocampus-dependent response less often (25%) and the visual cued response more often (75%) compared to WT littermates that used both strategies approximately equally. Hippocampal ID not only reduces spatial recognition memory performance but also affects systems that support procedural memory, suggesting an altered balance between memory systems. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-010-9049-0) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-010-9049-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.133-43[article] Hippocampus specific iron deficiency alters competition and cooperation between developing memory systems [Texte imprimé et/ou numérique] / E. S. CARLSON, Auteur ; S. J. FRETHAM, Auteur ; E. UNGER, Auteur ; M. O'CONNOR, Auteur ; A. PETRYK, Auteur ; T. SCHALLERT, Auteur ; R. RAO, Auteur ; I. TKAC, Auteur ; Michael K. GEORGIEFF, Auteur . - p.133-43.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.133-43
Mots-clés : DMT1, Slc11a2, Nuclear magnetic resonance spectroscopy Hippocampus Iron deficiency Memory systems Morris water maze Procedural memory Spatial memory Striatum Index. décimale : PER Périodiques Résumé : UNLABELLED: Iron deficiency (ID) is the most common gestational micronutrient deficiency in the world, targets the fetal hippocampus and striatum and results in long-term behavioral abnormalities. These structures primarily mediate spatial and procedural memory, respectively, in the rodent but have interconnections that result in competition or cooperation during cognitive tasks. We determined whether ID-induced impairment of one alters the function of the other by genetically inducing a 40% reduction of hippocampus iron content in late fetal life in mice and measuring dorsal striatal gene expression and metabolism and the behavioral balance between the two memory systems in adulthood. Slc11a2(hipp/hipp) mice had similar striatum iron content, but 18% lower glucose and 44% lower lactate levels, a 30% higher phosphocreatine:creatine ratio, and reduced iron transporter gene expression compared to wild type (WT) littermates, implying reduced striatal metabolic function. Slc11a2(hipp/hipp) mice had longer mean escape times on a cued task paradigm implying impaired procedural memory. Nevertheless, when hippocampal and striatal memory systems were placed in competition using a Morris Water Maze task that alternates spatial navigation and visual cued responses during training, and forces a choice between hippocampal and striatal strategies during probe trials, Slc11a2(hipp/hipp) mice used the hippocampus-dependent response less often (25%) and the visual cued response more often (75%) compared to WT littermates that used both strategies approximately equally. Hippocampal ID not only reduces spatial recognition memory performance but also affects systems that support procedural memory, suggesting an altered balance between memory systems. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-010-9049-0) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-010-9049-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 TPH2 polymorphisms and expression in Prader-Willi syndrome subjects with differing genetic subtypes / R. S. HENKHAUS in Journal of Neurodevelopmental Disorders, 2-3 (September 2010)
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[article]
Titre : TPH2 polymorphisms and expression in Prader-Willi syndrome subjects with differing genetic subtypes Type de document : Texte imprimé et/ou numérique Auteurs : R. S. HENKHAUS, Auteur ; D. C. BITTEL, Auteur ; M. G. BUTLER, Auteur Article en page(s) : p.144-8 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Prader-Willi syndrome (PWS) is a genetic imprinting disease that causes developmental and behavioral disturbances resulting from loss of expression of genes from the paternal chromosome 15q11-q13 region. In about 70% of subjects, this portion of the paternal chromosome is deleted, while 25% have two copies of the maternal chromosome 15, or uniparental maternal disomy (UPD; the remaining subjects have imprinting center defects. There are several documented physical and behavioral differences between the two major PWS genetic subtypes (deletion and UPD) indicating the genetic subtype plays a role in clinical presentation. Serotonin is known to be disturbed in PWS and affects both eating behavior and compulsion, which are reported to be abnormal in PWS. We investigated the tryptophan hydroxylase gene (TPH2), the rate-limiting enzyme in the production of brain serotonin, by analyzing three different TPH2 gene polymorphisms, transcript expression, and correlation with PWS genetic subtype. DNA and RNA from lymphoblastoid cell lines derived from 12 PWS and 12 comparison subjects were used for the determination of genetic subtype, TPH2 polymorphisms and quantitative RT-PCR analysis. A similar frequency of TPH2 polymorphisms was seen in the PWS and comparison subjects with PWS deletion subjects showing increased expression with one or more TPH2 polymorphism. Both PWS deletion and PWS UPD subjects had significantly lower TPH2 expression than control subjects and PWS deletion subjects had significantly lower TPH2 expression compared with PWS UPD subjects. PWS subjects with 15q11-q13 deletions had lower TPH2 expression compared with PWS UPD or control subjects, requiring replication and further studies to identify the cause including identification of disturbed gene interactions resulting from the deletion process. En ligne : http://dx.doi.org/10.1007/s11689-010-9051-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.144-8[article] TPH2 polymorphisms and expression in Prader-Willi syndrome subjects with differing genetic subtypes [Texte imprimé et/ou numérique] / R. S. HENKHAUS, Auteur ; D. C. BITTEL, Auteur ; M. G. BUTLER, Auteur . - p.144-8.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.144-8
Index. décimale : PER Périodiques Résumé : Prader-Willi syndrome (PWS) is a genetic imprinting disease that causes developmental and behavioral disturbances resulting from loss of expression of genes from the paternal chromosome 15q11-q13 region. In about 70% of subjects, this portion of the paternal chromosome is deleted, while 25% have two copies of the maternal chromosome 15, or uniparental maternal disomy (UPD; the remaining subjects have imprinting center defects. There are several documented physical and behavioral differences between the two major PWS genetic subtypes (deletion and UPD) indicating the genetic subtype plays a role in clinical presentation. Serotonin is known to be disturbed in PWS and affects both eating behavior and compulsion, which are reported to be abnormal in PWS. We investigated the tryptophan hydroxylase gene (TPH2), the rate-limiting enzyme in the production of brain serotonin, by analyzing three different TPH2 gene polymorphisms, transcript expression, and correlation with PWS genetic subtype. DNA and RNA from lymphoblastoid cell lines derived from 12 PWS and 12 comparison subjects were used for the determination of genetic subtype, TPH2 polymorphisms and quantitative RT-PCR analysis. A similar frequency of TPH2 polymorphisms was seen in the PWS and comparison subjects with PWS deletion subjects showing increased expression with one or more TPH2 polymorphism. Both PWS deletion and PWS UPD subjects had significantly lower TPH2 expression than control subjects and PWS deletion subjects had significantly lower TPH2 expression compared with PWS UPD subjects. PWS subjects with 15q11-q13 deletions had lower TPH2 expression compared with PWS UPD or control subjects, requiring replication and further studies to identify the cause including identification of disturbed gene interactions resulting from the deletion process. En ligne : http://dx.doi.org/10.1007/s11689-010-9051-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 Development and validation of the Arizona Cognitive Test Battery for Down syndrome / J. O. EDGIN in Journal of Neurodevelopmental Disorders, 2-3 (September 2010)
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[article]
Titre : Development and validation of the Arizona Cognitive Test Battery for Down syndrome Type de document : Texte imprimé et/ou numérique Auteurs : J. O. EDGIN, Auteur ; G. M. MASON, Auteur ; Melissa J. ALLMAN, Auteur ; George T. CAPONE, Auteur ; I. DELEON, Auteur ; C. MASLEN, Auteur ; R. H. REEVES, Auteur ; S. L. SHERMAN, Auteur ; L. NADEL, Auteur Article en page(s) : p.149-164 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Neurocognitive assessment in individuals with intellectual disabilities requires a well-validated test battery. To meet this need, the Arizona Cognitive Test Battery (ACTB) has been developed specifically to assess the cognitive phenotype in Down syndrome (DS). The ACTB includes neuropsychological assessments chosen to 1) assess a range of skills, 2) be non-verbal so as to not confound the neuropsychological assessment with language demands, 3) have distributional properties appropriate for research studies to identify genetic modifiers of variation, 4) show sensitivity to within and between sample differences, 5) have specific correlates with brain function, and 6) be applicable to a wide age range and across contexts. The ACTB includes tests of general cognitive ability and prefrontal, hippocampal and cerebellar function. These tasks were drawn from the Cambridge Neuropsychological Testing Automated Battery (CANTAB) and other established paradigms. Alongside the cognitive testing battery we administered benchmark and parent-report assessments of cognition and behavior. Individuals with DS (n=74, ages 7-38 years) and mental age (MA) matched controls (n=50, ages 3-8 years) were tested across 3 sites. A subsample of these groups were used for between-group comparisons, including 55 individuals with DS and 36 mental age matched controls. The ACTB allows for low floor performance levels and participant loss. Floor effects were greater in younger children. Individuals with DS were impaired on a number ACTB tests in comparison to a MA-matched sample, with some areas of spared ability, particularly on tests requiring extensive motor coordination. Battery measures correlated with parent report of behavior and development. The ACTB provided consistent results across contexts, including home vs. lab visits, cross-site, and among individuals with a wide range of socio-economic backgrounds and differences in ethnicity. The ACTB will be useful in a range of outcome studies, including clinical trials and the identification of important genetic components of cognitive disability. En ligne : http://dx.doi.org/10.1007/s11689-010-9054-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.149-164[article] Development and validation of the Arizona Cognitive Test Battery for Down syndrome [Texte imprimé et/ou numérique] / J. O. EDGIN, Auteur ; G. M. MASON, Auteur ; Melissa J. ALLMAN, Auteur ; George T. CAPONE, Auteur ; I. DELEON, Auteur ; C. MASLEN, Auteur ; R. H. REEVES, Auteur ; S. L. SHERMAN, Auteur ; L. NADEL, Auteur . - p.149-164.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.149-164
Index. décimale : PER Périodiques Résumé : Neurocognitive assessment in individuals with intellectual disabilities requires a well-validated test battery. To meet this need, the Arizona Cognitive Test Battery (ACTB) has been developed specifically to assess the cognitive phenotype in Down syndrome (DS). The ACTB includes neuropsychological assessments chosen to 1) assess a range of skills, 2) be non-verbal so as to not confound the neuropsychological assessment with language demands, 3) have distributional properties appropriate for research studies to identify genetic modifiers of variation, 4) show sensitivity to within and between sample differences, 5) have specific correlates with brain function, and 6) be applicable to a wide age range and across contexts. The ACTB includes tests of general cognitive ability and prefrontal, hippocampal and cerebellar function. These tasks were drawn from the Cambridge Neuropsychological Testing Automated Battery (CANTAB) and other established paradigms. Alongside the cognitive testing battery we administered benchmark and parent-report assessments of cognition and behavior. Individuals with DS (n=74, ages 7-38 years) and mental age (MA) matched controls (n=50, ages 3-8 years) were tested across 3 sites. A subsample of these groups were used for between-group comparisons, including 55 individuals with DS and 36 mental age matched controls. The ACTB allows for low floor performance levels and participant loss. Floor effects were greater in younger children. Individuals with DS were impaired on a number ACTB tests in comparison to a MA-matched sample, with some areas of spared ability, particularly on tests requiring extensive motor coordination. Battery measures correlated with parent report of behavior and development. The ACTB provided consistent results across contexts, including home vs. lab visits, cross-site, and among individuals with a wide range of socio-economic backgrounds and differences in ethnicity. The ACTB will be useful in a range of outcome studies, including clinical trials and the identification of important genetic components of cognitive disability. En ligne : http://dx.doi.org/10.1007/s11689-010-9054-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 Does bilateral damage to the human amygdala produce autistic symptoms? / L. K. PAUL in Journal of Neurodevelopmental Disorders, 2-3 (September 2010)
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[article]
Titre : Does bilateral damage to the human amygdala produce autistic symptoms? Type de document : Texte imprimé et/ou numérique Auteurs : L. K. PAUL, Auteur ; C. CORSELLO, Auteur ; D. TRANEL, Auteur ; Ralph ADOLPHS, Auteur Article en page(s) : p.165-173 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : A leading neurological hypothesis for autism postulates amygdala dysfunction. This hypothesis has considerable support from anatomical and neuroimaging studies. Individuals with bilateral amygdala lesions show impairments in some aspects of social cognition. These impairments bear intriguing similarity to those reported in people with autism, such as impaired recognition of emotion in faces, impaired theory of mind abilities, failure to fixate eyes in faces, and difficulties in regulating personal space distance to others. Yet such neurological cases have never before been assessed directly to see if they meet criteria for autism spectrum disorders (ASD). Here we undertook such an investigation in two rare participants with developmental-onset bilateral amygdala lesions. We administered a comprehensive clinical examination, as well as the Autism Diagnostic Observation Schedule (ADOS), the Social Responsiveness Scale (SRS), together with several other standardized questionnaires. Results from the two individuals with amygdala lesions were compared with published norms from both healthy populations as well as from people with ASD. Neither participant with amygdala lesions showed any evidence of autism across the array of different measures. The findings demonstrate that amygdala lesions in isolation are not sufficient for producing autistic symptoms. We suggest instead that it may be abnormal connectivity between the amygdala and other structures that contributes to autistic symptoms at a network level. En ligne : http://dx.doi.org/10.1007/s11689-010-9056-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.165-173[article] Does bilateral damage to the human amygdala produce autistic symptoms? [Texte imprimé et/ou numérique] / L. K. PAUL, Auteur ; C. CORSELLO, Auteur ; D. TRANEL, Auteur ; Ralph ADOLPHS, Auteur . - p.165-173.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.165-173
Index. décimale : PER Périodiques Résumé : A leading neurological hypothesis for autism postulates amygdala dysfunction. This hypothesis has considerable support from anatomical and neuroimaging studies. Individuals with bilateral amygdala lesions show impairments in some aspects of social cognition. These impairments bear intriguing similarity to those reported in people with autism, such as impaired recognition of emotion in faces, impaired theory of mind abilities, failure to fixate eyes in faces, and difficulties in regulating personal space distance to others. Yet such neurological cases have never before been assessed directly to see if they meet criteria for autism spectrum disorders (ASD). Here we undertook such an investigation in two rare participants with developmental-onset bilateral amygdala lesions. We administered a comprehensive clinical examination, as well as the Autism Diagnostic Observation Schedule (ADOS), the Social Responsiveness Scale (SRS), together with several other standardized questionnaires. Results from the two individuals with amygdala lesions were compared with published norms from both healthy populations as well as from people with ASD. Neither participant with amygdala lesions showed any evidence of autism across the array of different measures. The findings demonstrate that amygdala lesions in isolation are not sufficient for producing autistic symptoms. We suggest instead that it may be abnormal connectivity between the amygdala and other structures that contributes to autistic symptoms at a network level. En ligne : http://dx.doi.org/10.1007/s11689-010-9056-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 Maladaptive behaviors are linked with inefficient sleep in individuals with developmental disabilities / M. R. LENJAVI in Journal of Neurodevelopmental Disorders, 2-3 (September 2010)
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[article]
Titre : Maladaptive behaviors are linked with inefficient sleep in individuals with developmental disabilities Type de document : Texte imprimé et/ou numérique Auteurs : M. R. LENJAVI, Auteur ; Michael A. AHUJA, Auteur ; P. E. TOUCHETTE, Auteur ; Curt A. SANDMAN, Auteur Article en page(s) : p.174-180 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The purpose of the current study was to assess the relations between nightly sleep patterns and the frequency of daily maladaptive behavior. Antecedent and consequential relations between sleep patterns and behavior were evaluated with time series analysis. Sleep efficiency and maladaptive behavior were determined for 20 female residents of an institutional care facility for adults with developmental disabilities. Daily maladaptive behavioral data and nightly sleep/awake logs were collected for 4 months for each participant. Efficient sleep patterns were significantly associated with lower frequencies of maladaptive behaviors. All lagged cross-correlations 8 days before and 8 days after an evening of sleep were significant. These findings suggested that inefficient sleep was associated with increased maladaptive behaviors and that the lagged associations reflected a chronic but not an acute linkage between sleep and behavior. En ligne : http://dx.doi.org/10.1007/s11689-010-9048-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.174-180[article] Maladaptive behaviors are linked with inefficient sleep in individuals with developmental disabilities [Texte imprimé et/ou numérique] / M. R. LENJAVI, Auteur ; Michael A. AHUJA, Auteur ; P. E. TOUCHETTE, Auteur ; Curt A. SANDMAN, Auteur . - p.174-180.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.174-180
Index. décimale : PER Périodiques Résumé : The purpose of the current study was to assess the relations between nightly sleep patterns and the frequency of daily maladaptive behavior. Antecedent and consequential relations between sleep patterns and behavior were evaluated with time series analysis. Sleep efficiency and maladaptive behavior were determined for 20 female residents of an institutional care facility for adults with developmental disabilities. Daily maladaptive behavioral data and nightly sleep/awake logs were collected for 4 months for each participant. Efficient sleep patterns were significantly associated with lower frequencies of maladaptive behaviors. All lagged cross-correlations 8 days before and 8 days after an evening of sleep were significant. These findings suggested that inefficient sleep was associated with increased maladaptive behaviors and that the lagged associations reflected a chronic but not an acute linkage between sleep and behavior. En ligne : http://dx.doi.org/10.1007/s11689-010-9048-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342