1. Beuker KT, Schjolberg S, Lie KK, Donders R, Lappenschaar M, Swinkels SH, Buitelaar JK. {{The Structure of Autism Spectrum Disorder Symptoms in the General Population at 18 Months}}. {J Autism Dev Disord};2012 (May 5)
It is unclear whether symptoms of autism spectrum disorder (ASD) in young children in the population fit the three-factor structure of ASD as described in the DSM-IV, and cluster together in individual subjects. This study analysed questionnaire data on ASD symptoms filled in by mothers of 11,332 18-month-old children that was collected in the context of the Norwegian Mother and Child Cohort Study conducted by the Norwegian Institute of Public Health. Confirmatory Factor Analyses showed that the three-factor model had a significantly better fit then the two- and one-factor model of ASD symptoms. Latent class analysis revealed four homogeneous groups of children (classes) with different scores for Social Interaction and Communication at one hand and Stereotypies/Rigidity at the other hand.
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2. Borthwell RM, Hunsaker MR, Willemsen R, Berman RF. {{Spatiotemporal processing deficits in female CGG KI mice modeling the fragile X premutation}}. {Behav Brain Res};2012 (Apr 26)
The fragile X premutation is a tandem CGG trinucleotide repeat expansion in the fragile X mental retardation 1 (FMR1) gene between 55 and 200 repeats in length. A CGG knock-in (CGG KI) mouse has been developed that models the neuropathology and cognitive deficits reported in fragile X premutation carriers. It has been suggested that carriers of the premutation demonstrate a spatiotemporal hypergranularity, or reduced resolution of spatial and temporal processing. A temporal ordering of spatial locations task was used to evaluate the ability of CGG KI mice to process temporal and spatial information with either high or low levels of spatial interference. The results indicate that CGG KI mice showed difficulty performing a spatial novelty detection task when there were high levels of spatial interference, but were able to perform the novelty detection task when there was low spatial interference. These data suggest that CGG KI mice show reduced spatial and temporal resolution that are modulated by the dosage of the Fmr1 gene mutation, such that when behavioral tasks require mice to overcome high levels of either spatial or temporal interference, the CGG KI mice perform increasingly poorly as the CGG repeat length increases.
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3. Celestino-Soper PB, Violante S, Crawford EL, Luo R, Lionel AC, Delaby E, Cai G, Sadikovic B, Lee K, Lo C, Gao K, Person RE, Moss TJ, German JR, Huang N, Shinawi M, Treadwell-Deering D, Szatmari P, Roberts W, Fernandez B, Schroer RJ, Stevenson RE, Buxbaum JD, Betancur C, Scherer SW, Sanders SJ, Geschwind DH, Sutcliffe JS, Hurles ME, Wanders RJ, Shaw CA, Leal SM, Cook EH, Jr., Goin-Kochel RP, Vaz FM, Beaudet AL. {{A common X-linked inborn error of carnitine biosynthesis may be a risk factor for nondysmorphic autism}}. {Proc Natl Acad Sci U S A};2012 (May 7)
We recently reported a deletion of exon 2 of the trimethyllysine hydroxylase epsilon (TMLHE) gene in a proband with autism. TMLHE maps to the X chromosome and encodes the first enzyme in carnitine biosynthesis, 6-N-trimethyllysine dioxygenase. Deletion of exon 2 of TMLHE causes enzyme deficiency, resulting in increased substrate concentration (6-N-trimethyllysine) and decreased product levels (3-hydroxy-6-N-trimethyllysine and gamma-butyrobetaine) in plasma and urine. TMLHE deficiency is common in control males (24 in 8,787 or 1 in 366) and was not significantly increased in frequency in probands from simplex autism families (9 in 2,904 or 1 in 323). However, it was 2.82-fold more frequent in probands from male-male multiplex autism families compared with controls (7 in 909 or 1 in 130; P = 0.023). Additionally, six of seven autistic male siblings of probands in male-male multiplex families had the deletion, suggesting that TMLHE deficiency is a risk factor for autism (metaanalysis Z-score = 2.90 and P = 0.0037), although with low penetrance (2-4%). These data suggest that dysregulation of carnitine metabolism may be important in nondysmorphic autism; that abnormalities of carnitine intake, loss, transport, or synthesis may be important in a larger fraction of nondysmorphic autism cases; and that the carnitine pathway may provide a novel target for therapy or prevention of autism.
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4. Crosland K, Dunlap G. {{Effective Strategies for the Inclusion of Children With Autism in General Education Classrooms}}. {Behav Modif};2012 (May 3)
Successful inclusion of students with autism spectrum disorder (ASD) in general education classrooms can be challenging and may require additional supports. This article provides information on recent trends in autism intervention research and a review of research that has addressed individualized and systemic interventions for promoting inclusion. Response to intervention and schoolwide positive behavior support are reviewed as organizational/systems strategies relevant to preventing problems and improving social and academic outcomes for students with ASD. Additional individualized strategies that can be implemented within these models are described. A discussion of future research directions is provided.
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5. Dillenburger K. {{Why reinvent the wheel? A behaviour analyst’s reflections on pedagogy for inclusion for students with intellectual and developmental disability}}. {J Intellect Dev Disabil};2012 (Jun);37(2):169-180.
Abstract The number of children identified as having intellectual or developmental disability is rising worldwide and their education has been found wanting. It has been said that « they simply need better teaching. » At the same time, there is an increasing evidence base that pedagogy that is based on the discipline of behaviour analysis offers the best prospect for individuals diagnosed with autism spectrum disorders. On the basis of this evidence, it is proposed that behaviour analysis should be applied more broadly to improve teaching for all children with intellectual or developmental disability.
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6. Fendri-Kriaa N, Rouissi A, Ghorbel R, Mkaouar-Rebai E, Belguith N, Gouider-Khouja N, Fakhfakh F. {{Novel double deletions in the MECP2 gene in Tunisian Rett patient}}. {Gene};2012 (Apr 25)
Rett syndrome (RTT) is a severe neurodevelopmental disorder affecting almost exclusively girls. Rett patients present an apparently normal psychomotor development during the first 6-18months of life. Thereafter, they show a short period of developmental stagnation followed by a rapid regression in language and motor development. RTT is currently considered as monogenic X-linked dominant disorder due to mutations in the MECP2 gene, encoding the methyl-CpG binding protein 2. The aim of this study was to perform a mutational analysis of the MECP2 gene in a classical Rett patient.The results showed the presence of a novel point mutation c.C1142T (p.P381L) and two deletions at the heterozygous state: a novel deletion c.1075delTTC (p.S359) and a known one c.1157del44 (p.L386Q fs X2) in the C-terminal region of MeCP2.
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7. Grinker RR, Chambers N, Njongwe N, Lagman AE, Guthrie W, Stronach S, Richard BO, Kauchali S, Killian B, Chhagan M, Yucel F, Kudumu M, Barker-Cummings C, Grether J, Wetherby AM. {{« Communities » in Community Engagement: Lessons Learned From Autism Research in South Korea and South Africa}}. {Autism Res};2012 (May 4)
Little research has been conducted on behavioral characteristics of children with autism spectrum disorder (ASD) from diverse cultures within the US, or from countries outside of the US or Europe, with little reliable information yet reported from developing countries. We describe the process used to engage diverse communities in ASD research in two community-based research projects-an epidemiologic investigation of 7- to 12-year olds in South Korea and the Early Autism Project, an ASD detection program for 18- to 36-month-old Zulu-speaking children in South Africa. Despite the differences in wealth between these communities, ASD is underdiagnosed in both settings, and generally not reported in clinical or educational records. Moreover, in both countries, there is low availability of services. In both cases, local knowledge helped researchers to address both ethnographic as well as practical problems. Researchers identified the ways in which these communities generate and negotiate the cultural meanings of developmental disorders. Researchers incorporated that knowledge, as they engaged communities in a research protocol, adapted and translated screening and diagnostic tools, and developed methods for screening, evaluating, and diagnosing children with ASD. Autism Res 2012, **: **-**. (c) 2012 International Society for Autism Research, Wiley Periodicals, Inc.
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8. Hettinger JA, Liu X, Hudson ML, Lee A, Cohen IL, Michaelis RC, Schwartz CE, Lewis SM, Holden JJ. {{DRD2 and PPP1R1B (DARPP-32) polymorphisms independently confer increased risk for autism spectrum disorders and additively predict affected status in male-only affected sib-pair families}}. {Behav Brain Funct};2012 (May 4);8(1):19.
ABSTRACT: BACKGROUND: The neurotransmitter dopamine (DA) modulates executive functions, learning, and emotional processing, all of which are impaired in individuals with autism spectrum disorders (ASDs). Our previous findings suggest a role for dopamine-related genes in families with only affected males. METHODS: We examined two additional genes which affect DA function, the DRD2 and PPP1R1B (DARPP-32) genes, in a cohort of 112 male-only affected sib-pair families. Selected polymorphisms spanning these genes were genotyped and both family-based and population-based tests were carried out for association analysis. General discriminant analysis was used to examine the gene-gene interactions in predicting autism susceptibility. RESULTS: There was a significantly increased frequency of the DRD2 rs1800498TT genotype (P = 0.007) in affected males compared to the comparison group, apparently due to over-transmission of the T allele (P = 0.0003). The frequency of the PPP1R1B rs1495099CC genotype in affected males was also higher than that in the comparison group (P = 0.002) due to preferential transmission of the C allele from parents to affected children(P = 0.0009). Alleles rs1800498T and rs1495099C were associated with more severe problems in social interaction (P = 0.0002 and P = 0.0016, respectively) and communication (P = 0.0004 and P = 0.0046), and increased stereotypic behaviours (P = 0.0021 and P = 0.00072). General discriminant analysis found that the DRD2 and PPP1R1B genes additively predicted ASDs (P = 0.00011; Canonical R = 0.26) and explain ~7% of the variance in our families. All findings remained significant following corrections for multiple testing. CONCLUSION: Our findings support a role for the DRD2 and PPP1R1B genes in conferring risk for autism in families with only affected males and show an additive effect of these genes towards prediction of affected status in our families.
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9. Kandalaft MR, Didehbani N, Krawczyk DC, Allen TT, Chapman SB. {{Virtual Reality Social Cognition Training for Young Adults with High-Functioning Autism}}. {J Autism Dev Disord};2012 (May 9)
Few evidence-based social interventions exist for young adults with high-functioning autism, many of whom encounter significant challenges during the transition into adulthood. The current study investigated the feasibility of an engaging Virtual Reality Social Cognition Training intervention focused on enhancing social skills, social cognition, and social functioning. Eight young adults diagnosed with high-functioning autism completed 10 sessions across 5 weeks. Significant increases on social cognitive measures of theory of mind and emotion recognition, as well as in real life social and occupational functioning were found post-training. These findings suggest that the virtual reality platform is a promising tool for improving social skills, cognition, and functioning in autism.
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10. Pearson BL, Bettis JK, Meyza KZ, Yamamoto LY, Blanchard DC, Blanchard RJ. {{Absence of social conditioned place preference in BTBR T+tf/J mice: Relevance for social motivation testing in rodent models of autism}}. {Behav Brain Res};2012 (Apr 27)
A major goal of translation research in autism is to characterize the physiological and psychological processes underlying behavioral abnormalities. Since autism reflects impairments in social motivation, we modified the mouse three-chamber social approach apparatus for use as a social conditioned place preference arena. We paired one of two unique contexts with social interactions in juvenile mice for five or ten conditioning sessions in BTBR T+tf/J mice and a control strain with normal approach behaviors (C57BL/6J) since the BTBR T+tf/J inbred mouse strain displays a variety of behavioral alterations analogous to symptoms of autism spectrum disorders. While C57BL/6J mice formed a conditioned place preference to the context associated with social interactions, particularly those receiving ten days of conditioning, BTBR T+tf/J mice did not. Neither absence of social proximity nor avoidance due to high rates of autogrooming appeared to underlie the impaired positive incentive value of the unconditioned social stimulus in the BTBR T+tf/J strain. These data contribute to a growing body of evidence suggesting that the BTBR T+tf/J strain shows impairments in all diagnostic domains of autism including social motivation. Additionally, social conditioning testing might provide an important social motivation measure in other rodent models of neuropsychiatric disorders characterized by social abnormalities.
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11. Pennesi CM, Klein LC. {{Effectiveness of the gluten-free, casein-free diet for children diagnosed with autism spectrum disorder: Based on parental report}}. {Nutr Neurosci};2012 (Mar);15(2):85-91.
OBJECTIVES: Studies on the gluten-free and/or casein-free (GFCF) dietary intervention for children with autism spectrum disorders (ASDs) suggest that some children may positively respond to implementation of the dietary intervention. Other research suggests that children diagnosed with ASD can be classified into subpopulations based on various factors, including gastrointestinal (GI) abnormalities and immune function. METHODS: This study analyzes parental report data collected using a 90-item online questionnaire from 387 parents or primary caregivers of children diagnosed with ASD on the efficacy of the GFCF diet. Parents reported on their child’s GI symptoms, food allergy diagnoses, and suspected food sensitivities, as well as the degree and length of their diet implementation. RESULTS: Overall, diet efficacy among children whose parents reported the presence of GI symptoms, food allergy diagnoses, and suspected food sensitivities included greater improvement in ASD behaviors, physiological symptoms, and social behaviors compared with children whose parents reported none of these symptoms, diagnoses, or sensitivities (P < 0.05). Parental report of strict diet implementation, indicated by complete gluten/casein elimination and infrequent diet errors during and outside of parental care, also corresponded to improvement in ASD behaviors, physiological symptoms, and social behaviors (P < 0.05). DISCUSSION: These findings suggest that various intricacies related to diet implementation and GI and immune factors may play a role in differentiating diet responders from diet non-responders and substantiate the importance of further investigations into the various, nuanced factors that influence efficacy of the intervention among children with ASDs.
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12. Sahin M. {{Targeted treatment trials for tuberous sclerosis and autism: no longer a dream}}. {Curr Opin Neurobiol};2012 (May 3)
Genetic disorders that present with a high incidence of autism spectrum disorders (ASD) offer tremendous potential both for elucidating the underlying neurobiology of ASD and identifying therapeutic drugs and/or drug targets. As a result, clinical trials for genetic disorders associated with ASD are no longer a hope for the future but rather an exciting reality whose time has come. Tuberous sclerosis complex (TSC) is one such genetic disorder that presents with ASD, epilepsy, and intellectual disability. Cell culture and mouse model experiments have identified the mTOR pathway as a therapeutic target in this disease. This review summarizes the advantages of using TSC as model of ASD and the recent advances in the translational and clinical treatment trials in TSC.
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13. Sterling AM, Rice ML, Warren SF. {{Finiteness Marking in Boys with Fragile X Syndrome}}. {J Speech Lang Hear Res};2012 (May 4)
PURPOSE: The current study investigated finite marking (e.g., he walks, he walked) in boys with fragile X syndrome; the boys were grouped based on receptive vocabulary (i.e., borderline, impaired). METHOD: Twenty-one boys with the full mutation of fragile X, between the ages of 8 to 16 years participated. The boys completed probes from the Test of Early Grammatical Impairment (Rice & Wexler, 2001), a language sample, a nonverbal IQ test (Leiter-R, Roid & Miller, 1997), a receptive vocabulary test (PPVT-IV Dunn & Dunn, 2007), and a measure of autistic symptoms (CARS; Schopler et al., 2002). RESULTS: There were group differences for finiteness responses on the third person singular probe; the group with impaired vocabulary omitted markers with greater frequency compared to borderline vocabulary group. There were not significant differences on the past tense probe, with both groups performing lower than expectations based on receptive vocabulary ability. Nonverbal IQ was not correlated with the measures of finiteness marking. CONCLUSION: Boys with FXS demonstrate delays in finiteness marking, in particular on past tense verbs. Boys with FXS show a unique profile unlike children with SLI, in which their use of tense markers may exceed expectations benchmarked to clause length.
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14. Stone WS, Iguchi L. {{Do Apparent Overlaps between Schizophrenia and Autistic Spectrum Disorders Reflect Superficial Similarities or Etiological Commonalities?}}. {N Am J Med Sci (Boston)};2011 (Jul 25);4(3):124-133.
STUDY BACKGROUND: Schizophrenia and autism are both neurodevelopmental disorders that were once considered to be the same disorder expressed in different developmental periods. Although they were separated diagnostically about 40 years ago, they share several clinical and possibly, etiological features. This paper reviews overlaps in four domains of function to consider the issue of whether these similarities are sporadic and likely to represent superficial similarities, or whether the disorders are more likely to share some features in common. METHODS: Representative areas of function were reviewed and compared for aspects of cognition (nonverbal reasoning, memory and language), social function (orienting/joint attention, eye contact and theory of mind), brain function (structural differences) and genetics. To facilitate comparisons with schizophrenia, a focus on high functioning autism/Asperger’s disorder was utilized, particularly in the sections on cognition and social function. RESULTS: Significant similarities (and differences) characterized comparisons in each domain. CONCLUSIONS: Disturbed function in similar clinical (in cognition and social function), neurobiological (brain volumes) and genetic (e.g., involvement of the same genes or chromosomal locations) domains in autism and schizophrenia supports the hypothesis that while they are distinct disorders, they are not entirely unique. Additional studies of similarities and differences between them may thus shed light on common etiological mechanisms and hopefully, facilitate the development of novel treatment targets.
15. Talos DM, Sun H, Zhou X, Fitzgerald EC, Jackson MC, Klein PM, Lan VJ, Joseph A, Jensen FE. {{The Interaction between Early Life Epilepsy and Autistic-Like Behavioral Consequences: A Role for the Mammalian Target of Rapamycin (mTOR) Pathway}}. {PLoS One};2012;7(5):e35885.
Early life seizures can result in chronic epilepsy, cognitive deficits and behavioral changes such as autism, and conversely epilepsy is common in autistic children. We hypothesized that during early brain development, seizures could alter regulators of synaptic development and underlie the interaction between epilepsy and autism. The mammalian Target of Rapamycin (mTOR) modulates protein translation and is dysregulated in Tuberous Sclerosis Complex, a disorder characterized by epilepsy and autism. We used a rodent model of acute hypoxia-induced neonatal seizures that results in long term increases in neuronal excitability, seizure susceptibility, and spontaneous seizures, to determine how seizures alter mTOR Complex 1 (mTORC1) signaling. We hypothesized that seizures occurring at a developmental stage coinciding with a critical period of synaptogenesis will activate mTORC1, contributing to epileptic networks and autistic-like behavior in later life. Here we show that in the rat, baseline mTORC1 activation peaks during the first three postnatal weeks, and induction of seizures at postnatal day 10 results in further transient activation of its downstream targets phospho-4E-BP1 (Thr37/46), phospho-p70S6K (Thr389) and phospho-S6 (Ser235/236), as well as rapid induction of activity-dependent upstream signaling molecules, including BDNF, phospho-Akt (Thr308) and phospho-ERK (Thr202/Tyr204). Furthermore, treatment with the mTORC1 inhibitor rapamycin immediately before and after seizures reversed early increases in glutamatergic neurotransmission and seizure susceptibility and attenuated later life epilepsy and autistic-like behavior. Together, these findings suggest that in the developing brain the mTORC1 signaling pathway is involved in epileptogenesis and altered social behavior, and that it may be a target for development of novel therapies that eliminate the progressive effects of neonatal seizures.
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16. von dem Hagen EA, Stoyanova RS, Baron-Cohen S, Calder AJ. {{Reduced functional connectivity within and between ‘social’ resting state networks in Autism Spectrum Conditions}}. {Soc Cogn Affect Neurosci};2012 (May 3)
Individuals with Autism Spectrum Conditions (ASC) have difficulties in social interaction and communication, which is reflected in hypoactivation of brain regions engaged in social processing, such as medial prefrontal cortex (mPFC), amygdala and insula. Resting state studies in ASC have identified reduced connectivity of the default mode network (DMN), which includes mPFC, suggesting that other resting state networks incorporating ‘social’ brain regions may also be abnormal. Using Seed-based Connectivity and Group Independent Component Analysis (ICA) approaches, we looked at resting functional connectivity in ASC between specific ‘social’ brain regions, as well as within and between whole networks incorporating these regions. We found reduced functional connectivity within the DMN in individuals with ASC, using both ICA and seed-based approaches. Two further networks identified by ICA, the salience network, incorporating the insula, and a medial temporal lobe network, incorporating the amygdala, showed reduced inter-network connectivity. This was underlined by reduced seed-based connectivity between the insula and amygdala. The results demonstrate significantly reduced functional connectivity within and between resting state networks incorporating ‘social’ brain regions. This reduced connectivity may result in difficulties in communication and integration of information across these networks, which could contribute to the impaired processing of social signals in ASC.
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17. Wegiel J, Frackowiak J, Mazur-Kolecka B, Schanen NC, Cook EH, Jr., Sigman M, Brown WT, Kuchna I, Nowicki K, Imaki H, Ma SY, Chauhan A, Chauhan V, Miller DL, Mehta PD, Flory M, Cohen IL, London E, Reisberg B, de Leon MJ, Wisniewski T. {{Abnormal Intracellular Accumulation and Extracellular Abeta Deposition in Idiopathic and Dup15q11.2-q13 Autism Spectrum Disorders}}. {PLoS One};2012;7(5):e35414.
BACKGROUND: It has been shown that amyloid ss (Abeta), a product of proteolytic cleavage of the amyloid beta precursor protein (APP), accumulates in neuronal cytoplasm in non-affected individuals in a cell type-specific amount. METHODOLOGY/PRINCIPAL FINDINGS: In the present study, we found that the percentage of amyloid-positive neurons increases in subjects diagnosed with idiopathic autism and subjects diagnosed with duplication 15q11.2-q13 (dup15) and autism spectrum disorder (ASD). In spite of interindividual differences within each examined group, levels of intraneuronal Abeta load were significantly greater in the dup(15) autism group than in either the control or the idiopathic autism group in 11 of 12 examined regions (p<0.0001 for all comparisons; Kruskall-Wallis test). In eight regions, intraneuronal Abeta load differed significantly between idiopathic autism and control groups (p<0.0001). The intraneuronal Abeta was mainly N-terminally truncated. Increased intraneuronal accumulation of Abeta(17-40/42) in children and adults suggests a life-long enhancement of APP processing with alpha-secretase in autistic subjects. Abeta accumulation in neuronal endosomes, autophagic vacuoles, Lamp1-positive lysosomes and lipofuscin, as revealed by confocal microscopy, indicates that products of enhanced alpha-secretase processing accumulate in organelles involved in proteolysis and storage of metabolic remnants. Diffuse plaques containing Abeta(1-40/42) detected in three subjects with ASD, 39 to 52 years of age, suggest that there is an age-associated risk of alterations of APP processing with an intraneuronal accumulation of a short form of Abeta and an extracellular deposition of full-length Abeta in nonfibrillar plaques. CONCLUSIONS/SIGNIFICANCE: The higher prevalence of excessive Abeta accumulation in neurons in individuals with early onset of intractable seizures, and with a high risk of sudden unexpected death in epilepsy in autistic subjects with dup(15) compared to subjects with idiopathic ASD, supports the concept of mechanistic and functional links between autism, epilepsy and alterations of APP processing leading to neuronal and astrocytic Abeta accumulation and diffuse plaque formation.
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18. Woodman AC, Hauser-Cram P. {{The role of coping strategies in predicting change in parenting efficacy and depressive symptoms among mothers of adolescents with developmental disabilities}}. {J Intellect Disabil Res};2012 (May 8)
Background Parents of children with developmental disabilities (DD) face greater caregiving demands than parents of children without DD. There is considerable variability in parents’ adjustment to raising a child with DD, however. In line with a strengths-based approach, this study explores coping strategies as potential mechanisms of resilience among mothers of adolescents with DD. This study examines the frequency with which mothers use various coping strategies and the extent to which those strategies moderate the relationship between adolescent behaviour problems and aspects of maternal well-being. Both positive and negative dimensions of well-being are explored, with maternal depressive symptoms and perceived parenting efficacy examined as outcomes cross-sectionally and longitudinally. Methods The present study focuses on 92 mothers and their adolescents with DD. The adolescents had a wide range of diagnoses, all with continuing special needs. Data were collected from mothers through interviews and self-administered questionnaires when their adolescents were aged 15 and aged 18. A structured assessment of the adolescent was completed during home visits at age 15. Results Mothers reported frequently using strategies of denial and planning but rarely using strategies of mental and behavioural disengagement to cope with recent stressful situations. Adolescent behaviour problems were found to contribute to greater symptoms of depression and lower feelings of parenting efficacy as well as increases in depressive symptoms over time. Mothers of sons, but not daughters, reported increases in parenting efficacy across their child’s adolescent period. Above and beyond adolescent factors, several coping strategies emerged as significant predictors of mothers’ symptoms of depression and perceived parenting efficacy. Moreover, use of Active Coping/Planning, Positive Reinterpretation/Growth, and Behavioural/Mental Disengagement as coping strategies moderated the impact of adolescent behaviour problems on maternal depressive symptoms. Conclusions This study extends previous findings by focusing on both positive and negative dimensions of parent well-being during their child’s adolescent period. Adolescence can be a stressful time for parents, with typical developmental tasks entailing additional strains for parents of adolescents with DD. The present findings point to several coping strategies that may reduce the impact of challenging behaviours during this period on mothers’ symptoms of depression and feelings of parenting efficacy. Certain coping strategies were found to exert a greater impact on maternal well-being for parents of adolescents with higher levels of behaviour problems, suggesting that interventions may benefit from an increased focus on this group of mothers with heightened caregiving demands.
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19. Zerbo O, Iosif AM, Walker C, Ozonoff S, Hansen RL, Hertz-Picciotto I. {{Is Maternal Influenza or Fever During Pregnancy Associated with Autism or Developmental Delays? Results from the CHARGE (CHildhood Autism Risks from Genetics and Environment) Study}}. {J Autism Dev Disord};2012 (May 5)
We analyzed data from case groups of 538 children with autism spectrum disorders (ASD) and 163 with developmental delays (DD), and from 421 typically developing controls to assess associations with maternal influenza or fever during pregnancy. Exposure information was obtained by telephone interviews, and outcomes were clinically confirmed. Though neither ASD nor DD was associated with influenza, both were associated with maternal fever during pregnancy: OR’s (odds ratios) were 2.12 (95 % CI 1.17, 3.84) and 2.50 (95 % CI 1.20, 5.20) respectively. However, the fever-associated ASD risk was attenuated among mothers who reported taking antipyretic medications (OR = 1.30, 95 % CI 0.59, 2.84), but remained elevated for those who did not (OR = 2.55, 95 % CI 1.30, 4.99).
