Differentiation of retardation and autism from specific communication disorders.
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INTRODUCTION: Analysis of nocturnal sleep in infantile autism has been presented in various studies. However, there has been no systematization including the different structural and paroxystic alterations at the same time as permitting the development of a general theory of the effect of sleep on prognosis and treatment, particularly in a spectrum in which there is currently no definite solution. DEVELOPMENT: A systematic review was made of the literature obtained from publications included in MEDLINE and web pages of the last 25 years using the key words: autism, Asperger's disorder, sleep, childhood and Rett's syndrome. Altogether 21 papers fulfllled criteria for inclusion. Disorders of sleep in infantile autism were classified into three types: immaturity of sleep, showing a destructured polysomnographic recording and negative correlation with the level of development; functional alterations of sleep with early waking and difficulty in going to sleep being the disorders most frequently seen; and paroxystic alterations with epileptiform discharges being the commonest, without necessarily occurring together with seizures. The opinions stated on questionnaires and the data observed on the polysomnography were not in agreement. CONCLUSIONS: Analysis of the literature has permitted us to make an initial classification of sleep disorders in autistic children, and has shown a marked presence of these disorders in the evolution of autistic children. It is necessary that further studies being done, polysomnographic rather than by means of questionnaires, for two reasons: clinical and in order to obtain more precise classification.
BACKGROUND: Reliable, valid and easily administered screening instruments would greatly facilitate large-scale neuropsychiatric research. AIMS: To test a parent telephone interview focused on autism - tics, attention-deficit hyperactivity disorder (ADHD) and other comorbidities (A-TAC). METHOD: Parents of 84 children in contact with a child neuropsychiatric clinic and 27 control children were interviewed. Validity and interrater and test - retest reliability were assessed. RESULTS: Interrater and test - retest reliability were very good. Areas under receiver operating characteristics curves between interview scores and clinical diagnoses were around 0.90 for ADHD and autistic spectrum disorders, and above 0.70 for tics, learning disorders and developmental coordination disorder. Using optimal cut-off scores for autistic spectrum disorder and ADHD, good to excellent kappa levels for interviews and clinical diagnoses were noted. CONCLUSIONS: The A-TAC appears to be a reliable and valid instrument for identifying autistic spectrum disorder, ADHD, tics, learning disorders and developmental coordination disorder.
Coincident cases of Tourette syndrome and Pervasive Developmental Disorders increasingly have been reported in the literature. Coincident cases currently number around 90. A minority of cases have been associated with cases of Tourette syndrome and tics in other family members; this has led some authors to suggest that Tourette syndrome may be responsible for some of the genetic heterogeneity in Pervasive Developmental Disorders. The literature is reviewed, along with some aspects of the neurobiology of the two conditions with arguments for and against this hypothesis.
Autism is a neurodevelopmental disorder characterized by dysfunction in three core behavioral domains: repetitive behaviors, social deficits, and language abnormalities. There is evidence that abnormalities exist in peptide systems, particularly the oxytocin system, in autism spectrum patients. Furthermore, oxytocin and the closely related peptide vasopressin are known to play a role in social and repetitive behaviors. This study examined the impact of oxytocin on repetitive behaviors in 15 adults with autism or Asperger's disorder via randomized double-blind oxytocin and placebo challenges. The primary outcome measure was an instrument rating six repetitive behaviors: need to know, repeating, ordering, need to tell/ask, self-injury, and touching. Patients with autism spectrum disorders showed a significant reduction in repetitive behaviors following oxytocin infusion in comparison to placebo infusion. Repetitive behavior in autism spectrum disorders may be related to abnormalities in the oxytocin system, and may be partially ameliorated by synthetic oxytocin infusion.
In 2002, we published a paper [Brock, J., Brown, C., Boucher, J., Rippon, G., 2002. The temporal binding deficit hypothesis of autism. Development and Psychopathology 142, 209-224] highlighting the parallels between the psychological model of 'central coherence' in information processing [Frith, U., 1989. Autism: Explaining the Enigma. Blackwell, Oxford] and the neuroscience model of neural integration or 'temporal binding'. We proposed that autism is associated with abnormalities of information integration that is caused by a reduction in the connectivity between specialised local neural networks in the brain and possible overconnectivity within the isolated individual neural assemblies. The current paper updates this model, providing a summary of theoretical and empirical advances in research implicating disordered connectivity in autism. This is in the context of changes in the approach to the core psychological deficits in autism, of greater emphasis on 'interactive specialisation' and the resultant stress on early and/or low-level deficits and their cascading effects on the developing brain [Johnson, M.H., Halit, H., Grice, S.J., Karmiloff-Smith, A., 2002. Neuroimaging of typical and atypical development: a perspective from multiple levels of analysis. Development and Psychopathology 14, 521-536]. We also highlight recent developments in the measurement and modelling of connectivity, particularly in the emerging ability to track the temporal dynamics of the brain using electroencephalography (EEG) and magnetoencephalography (MEG) and to investigate the signal characteristics of this activity. This advance could be particularly pertinent in testing an emerging model of effective connectivity based on the balance between excitatory and inhibitory cortical activity [Rubenstein, J.L., Merzenich M.M., 2003. Model of autism: increased ratio of excitation/inhibition in key neural systems. Genes, Brain and Behavior 2, 255-267; Brown, C., Gruber, T., Rippon, G., Brock, J., Boucher, J., 2005. Gamma abnormalities during perception of illusory figures in autism. Cortex 41, 364-376]. Finally, we note that the consequence of this convergence of research developments not only enables a greater understanding of autism but also has implications for prevention and remediation.
INTRODUCTION: Hyperlexia is described in children who present alterations or retardation in development and is frequently characterised by their teaching themselves to read at an early age. This ability to decode words does not correlate with their intellectual level and can course with different degrees of mental retardation. It is always accompanied by difficulty in establishing social relationships. Autism is a disorder that is prototypical of the autistic spectrum disorders (ASD), which are essentially characterised by qualitative alterations in social interaction, in communication and language development, and in the presence of a limited repertory of interests, accompanied by stereotyped or peculiar responses. METHOD: The presence of hyperlexia in autistic children is more frequent than in other development disorders. This phenomenon is linked with the increased skills involving visual memory, visual discrimination and motivation/interest towards visually represented material that is to be found in people with autism. However, not all autistic individuals present hyperlexia and not all children with hyperlexia present autism, although evidence shows that hyperlexia is a phenomenon that is observed with greater frequency in autism and in ASD. CONCLUSION: Hyperlexia, understood as meaning a little island of ability in children with autism and ASD, poses a number of questions and represents an important challenge in neuropsychological research in this population.
There is consensus about the disorders that comprise the autistic spectrum, with autistic disorder, Asperger's disorder, and PDD-NOS as the most typical examples and Rett's disorder and disintegrative disorder as the other components. Important controversies regarding the precise definitions of autistic spectrum disorders and the boundaries between the milder manifestations of those disorders, particularly PDD-NOS, and non-autistic conditions have not been and cannot be resolved fully as long as there is no known biologic cause or consistent biologic or psychological marker. This includes issues as basic as whether the autistic spectrum is a predominantly unitary entity or a collection of more or less similar phenotypes with multiple, varying etiologies. This is why the highest long-term priority in the area of definite diagnosis is the search for biologic marker(s) for autism and related autism spectrum disorders [91]. In the absence of a medical test to unequivocally diagnose autism, definitions of autism and related conditions are based only on manifestations in overt behavior, with all the unreliability this entails. In the future, the discovery of biologic correlates, causes, and pathogenetic pathways will undoubtedly change the way in which autism is diagnosed and lead to a new nosology [95]. Until that time the definitions in the current versions of the classification systems should be considered in a state of evolution. The key problem of the current classification systems is the fact that the boundaries between the various disorders are fuzzy. Instead of a categorical approach, a more useful description might be that of "autistic spectrum disorder," which reflects the range of severity of symptoms. Such a dimensional understanding of PDD is useful to clinicians, who may otherwise use nonspecific terms to avoid the categorical diagnosis of autism [31]. Rutter and Schopler [96] argued for separate clinical and research schemes because clinical and research needs are different. For research purposes it is desirable to have as much direct comparability across studies as possible. The focus is on a high degree of homogeneity within diagnostic groupings. A price must be paid for this detailed specification, and the main cost lies in the proportion of cases left undiagnosed. For example, there may be good scientific reasons for a narrowly defined categorical diagnosis that includes only individuals who definitely and clearly have a specifically defined condition and excludes individuals who may have the condition. For clinicians and educators, classification helps guide the selection of treatments for an individual. From this point of view, broader diagnostic concepts may be most appropriate [95].
BACKGROUND: The recorded prevalence of autistic spectrum disorders has risen over recent decades. Measles, mumps and rubella (MMR) vaccine has been blamed, by causing a "new variant" form of "regressive autism" associated with "autistic enterocolitis". AIMS: To estimate the prevalence of autism and to assess any changes in parental perception regarding the onset or causes of autism. METHODS AND RESULTS: A total of 567 children with autistic spectrum disorder in five districts in north east London were identified, born 1979-98. Reported autism, excluding the 94 cases of Asperger's syndrome, increased by year of birth until 1992, since when prevalence has plateaued. This flattening off persisted after allowing for expected delay in diagnosis in more recent birth cohorts. The age at diagnosis of autistic spectrum disorder was estimated to have decreased per five year period since 1983, by 8.7% for childhood autism and by 11.0% for atypical autism. There was some evidence that MMR was more likely to be mentioned as a trigger after August 1997 than before. CONCLUSIONS: The prevalence of autism, which was apparently rising from 1979 to 1992, reached a plateau from 1992 to 1996 at a rate of some 2.6 per 1000 live births. This levelling off, together with the reducing age at diagnosis, suggests that the earlier recorded rise in prevalence was not a real increase but was likely due to factors such as increased recognition, a greater willingness on the part of educationalists and families to accept the diagnostic label, and better recording systems. The proportion of parents attributing their child's autism to MMR appears to have increased since August 1997.
Compared 8- to 14-year-old children with either autism or receptive developmental language disorder (RDLD) to age- and IQ-matched normal controls in their ability to detect both frequent (p = .70) and infrequent (p = .30) randomly presented auditory stimuli under task and no-task conditions. Event-related brain potentials (ERPs), behavioral reaction times, and target detection accuracy rates were measured. Although the three groups of children performed in a similar manner on behavioral measures, only the children with autism demonstrated an abnormally small amplitude of the P3b, a component of the ERP. This result is interpreted in terms of (a) the consistency of this finding with other ERP studies involving older individuals with autism; and (b) its significance with respect to the difficulty children with autism have in modifying their expectancies to contextually relevant sequences of auditory information.