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Sökning: WFRF:(Gillberg Christopher 1950 )

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1.
  • Gillberg, Christopher, 1950, et al. (författare)
  • Mortality in autism: a prospective longitudinal community-based study.
  • 2010
  • Ingår i: Journal of Autism and Developmental Disorders. - : Springer Science and Business Media LLC. - 0162-3257 .- 1573-3432. ; 40:3, s. 352-357
  • Tidskriftsartikel (refereegranskat)abstract
    • The purposes of the present study were to establish the mortality rate in a representative group of individuals (n = 120) born in the years 1962-1984, diagnosed with autism/atypical autism in childhood and followed up at young adult age (>/=18 years of age), and examine the risk factors and causes of death. The study group, which constituted a total population sample of children with these diagnoses, were followed up in Swedish registers. Nine (7.5%) of the 120 individuals with autism had died at the time of follow-up, a rate 5.6 times higher than expected. The mortality rate was significantly higher among the females. Associated medical disorders (including epilepsy with cognitive impairment) and accidents accounted for most of the deaths, and it was not possible to determine whether autism "per se" actually carries an increased mortality risk.
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2.
  • Hadjikhani, Nouchine, 1966, et al. (författare)
  • Emotional contagion for pain is intact in autism spectrum disorders.
  • 2014
  • Ingår i: Translational psychiatry. - : Springer Science and Business Media LLC. - 2158-3188. ; 4
  • Tidskriftsartikel (refereegranskat)abstract
    • Perceiving others in pain generally leads to empathic concern, consisting of both emotional and cognitive processes. Empathy deficits have been considered as an element contributing to social difficulties in individuals with autism spectrum disorders (ASD). Here, we used functional magnetic resonance imaging and short video clips of facial expressions of people experiencing pain to examine the neural substrates underlying the spontaneous empathic response to pain in autism. Thirty-eight adolescents and adults of normal intelligence diagnosed with ASD and 35 matched controls participated in the study. In contrast to general assumptions, we found no significant differences in brain activation between ASD individuals and controls during the perception of pain experienced by others. Both groups showed similar levels of activation in areas associated with pain sharing, evidencing the presence of emotional empathy and emotional contagion in participants with autism as well as in controls. Differences between groups could be observed at a more liberal statistical threshold, and revealed increased activations in areas involved in cognitive reappraisal in ASD participants compared with controls. Scores of emotional empathy were positively correlated with brain activation in areas involved in embodiment of pain in ASD group only. Our findings show that simulation mechanisms involved in emotional empathy are preserved in high-functioning individuals with autism, and suggest that increased reappraisal may have a role in their apparent lack of caring behavior.
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3.
  • Wentz, Elisabet, 1964, et al. (författare)
  • Bone density 11 years after anorexia nervosa onset in a controlled study of 39 cases.
  • 2003
  • Ingår i: International Journal of Eating Disorders. - 0276-3478. ; 34:3, s. 314-318
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective To evaluate bone mineral density (BMD) and body composition 11 years after the onset of anorexia nervosa (AN). Method Thirty-nine AN subjects (36 females, 3 males), selected from a population-based sample, and 46 matched controls (COMP; 43 females, 3 males) were examined by using double-energy X-ray absorptiometry (DXA). Only 2 women still had AN. None of the men had AN. Results The females in the AN and COMP groups did not differ regarding BMD, nor was there a difference across female groups concerning body mass index (BMI). The female AN group had a significantly lower percentage of body fat. BMD among females in the AN group was related to lowest BMI ever. There was an inverse relationship between lumbar BMD and AN duration. Discussion Low BMD is not overrepresented among weight-restored AN patients at long-term follow-up compared with healthy women. However, the inverse relationship between BMD and AN duration may be indicative of a risk for osteopenia in patients with subchronic and chronic AN.
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5.
  • Allely, Clare S, et al. (författare)
  • Can psychopathology at age 7 be predicted from clinical observation at one year? Evidence from the ALSPAC cohort.
  • 2012
  • Ingår i: Research in Developmental Disabilities. - : Elsevier BV. - 0891-4222. ; 33:6, s. 2292-2300
  • Tidskriftsartikel (refereegranskat)abstract
    • One of the challenges of developmental psychopathology is to determine whether identifiable pathways to developmental disorders exist in the first months or years of life. Early identification of such disorders poses a similar challenge for clinical services. Using data from a large contemporary birth cohort, we examined whether psychopathology at age seven can be predicted from clinician observation at one year. Two groups of clinical raters observed videos of caregiver-infant interaction. Neither group of raters could reliably identify any precursors of later development of psychopathology in the one-year-old infants in this setting.
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6.
  • Anckarsäter, Henrik, 1966, et al. (författare)
  • Child neurodevelopmental and behavioural problems are intercorrelated and dimensionally distributed in the general population
  • 2008
  • Ingår i: The Open Psychiatry Journal. - : Bentham Science Publishers Ltd.. - 1874-3544. ; 2, s. 5-11
  • Tidskriftsartikel (refereegranskat)abstract
    • The Autism – Tics, AD/HD, and other Comorbidities inventory (A-TAC) is a comprehensive interview for evaluating problems related to autism spectrum disorders (ASD), tic disorders, attention-deficit/hyperactivity disorder (AD/HD), and common comorbid conditions in children and adolescents. A-TAC telephone interviews were administered to parents of 2,957 children aged nine- or twelve-years, representing one in each twin pair included in the population- based Child and Adolescent Twin Study in Sweden (CATSS). A total of 16.4% were screen-positive for one or several of the targeted disorder, 1.3% for ASD and 5.6% for AD/HD. All types of problems were more common among boys, with the exception of those related to “eating habits”. They were all dimensionally/continuously distributed, highly inter-correlated, and overlapped across types. They aggregated in three ba- sic factors corresponding to externalizing/disruptiveness, socio-communicative problems, and compulsiveness. Population-based data on problems in children thus challenge current categorical diagnostic definitions, calling for dimen- sional and complementary models of problem descriptions.
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7.
  • Anckarsäter, Henrik, et al. (författare)
  • The sociocommunicative deficit subgroup in anorexia nervosa: autism spectrum disorders and neurocognition in a community-based, longitudinal study
  • 2012
  • Ingår i: Psychological Medicine. - 1469-8978 .- 0033-2917. ; 42:9, s. 1957-1967
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: A subgroup of persons with anorexia nervosa (AN) have been proposed to have sociocommunicative problems corresponding to autism spectrum disorders [ASDs, i.e. DSM-IV pervasive developmental disorders (PDDs): autistic disorder, Asperger's disorder, PDD not otherwise specified (NOS)]. Here, clinical problems, personality traits, cognitive test results and outcome are compared across 16 subjects (32%) with teenage-onset AN who meet or have met ASD criteria (AN+ASD), 34 ASD-negative AN subjects and matched controls from a longitudinal Swedish study including four waves of independent assessments from the teens to the early thirties.MethodThe fourth wave included the Structured Clinical Interview for DSM-IV (SCID)-I and the SCID-II (cluster C, i.e. 'anxious' PDs) interviews, the Asperger Syndrome Diagnostic Interview, self-assessments by the Autism Spectrum Quotient and the Temperament and Character Inventory, neurocognitive tests by subscales from the Wechsler scales, continuous performance tests, Tower of London, and Happé's cartoons. RESULTS: The ASD assessments had substantial inter-rater reliability over time (Cohen's κ between 0.70 and 0.80 with previous assessments), even if only six subjects had been assigned a diagnosis of an ASD in all four waves of the study, including retrospective assessments of pre-AN neurodevelopmental problems. The AN+ASD group had the highest prevalence of personality disorders and the lowest Morgan-Russell scores. The non-ASD AN group also differed significantly from controls on personality traits related to poor interpersonal functioning and on neurocognitive tests. CONCLUSIONS: A subgroup of subjects with AN meet criteria for ASDs. They may represent the extreme of neurocognitive and personality problems to be found more generally in AN.
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8.
  • Anney, Richard, et al. (författare)
  • A genome-wide scan for common alleles affecting risk for autism.
  • 2010
  • Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 19:20, s. 4072-4082
  • Tidskriftsartikel (refereegranskat)abstract
    • Although autism spectrum disorders (ASDs) have a substantial genetic basis, most of the known genetic risk has been traced to rare variants, principally copy number variants (CNVs). To identify common risk variation, the Autism Genome Project (AGP) Consortium genotyped 1558 rigorously defined ASD families for 1 million single-nucleotide polymorphisms (SNPs) and analyzed these SNP genotypes for association with ASD. In one of four primary association analyses, the association signal for marker rs4141463, located within MACROD2, crossed the genome-wide association significance threshold of P < 5 × 10(-8). When a smaller replication sample was analyzed, the risk allele at rs4141463 was again over-transmitted; yet, consistent with the winner's curse, its effect size in the replication sample was much smaller; and, for the combined samples, the association signal barely fell below the P < 5 × 10(-8) threshold. Exploratory analyses of phenotypic subtypes yielded no significant associations after correction for multiple testing. They did, however, yield strong signals within several genes, KIAA0564, PLD5, POU6F2, ST8SIA2 and TAF1C.
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9.
  • Anney, Richard, et al. (författare)
  • Individual common variants exert weak effects on the risk for autism spectrum disorders.
  • 2012
  • Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 21:21, s. 4781-92
  • Tidskriftsartikel (refereegranskat)abstract
    • While it is apparent that rare variation can play an important role in the genetic architecture of autism spectrum disorders (ASD), the contribution of common variation to ASD risk is less clear. To produce a more comprehensive picture, we report Stage 2 of the Autism Genome Project genome-wide association study, adding 1301 ASD families and bringing the total to 2705 families analysed (Stages 1 and 2). In addition to evaluating association of individual SNPs, we also sought evidence that common variants, en masse, might affect risk. Despite genotyping over a million SNPs covering the genome, no single SNP shows significant association with ASD or selected phenotypes at a genome-wide level. The SNP that achieves the smallest p-value from secondary analyses is rs1718101. It falls in CNTNAP2, a gene previously implicated in susceptibility for ASD. This SNP also shows modest association with age of word/phrase acquisition in ASD subjects, of interest because features of language development are also associated with other variation in CNTNAP2. By contrast, allele-scores derived from the transmission of common alleles to Stage 1 cases significantly predict case-status in the independent Stage 2 sample. Despite being significant, the variance explained by these allele scores was small (Vm< 1%). Based on results from individual SNPs and their en masse effect on risk, as inferred from the allele-score results, it is reasonable to conclude that common variants affect ASD risk but their individual effects are modest.
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