Abnormal Neuroanatomy in a Nonretarded Person With Autism

Courchesne, Eric

doi:10.1001/archneur.1987.00520150073028

Cited by 144 publications

(19 citation statements)

References 34 publications

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“…This finding has not been reported before in autistic subjects probably as other studies have typically not corrected brain volume (Courchesne et al, 1987;Gaffney et al, 1989;Howard et al, 2000;Piven et al, 1995;Townsend et al, 2001). However, percent brain enlargement was 1.3-6.7% in those studies (Howard et al, 2000;Piven et al, 1995;Townsend et al, 2001), whereas ventricular enlargement was 28.9-153%.…”

Section: Discussionmentioning

confidence: 59%

Larger Brains in Medication Naive High-Functioning Subjects with Pervasive Developmental Disorder

Palmen

Pol

Kemner

et al. 2004

J Autism Dev Disord

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Section: Discussionmentioning

confidence: 59%

Larger Brains in Medication Naive High-Functioning Subjects with Pervasive Developmental Disorder

Palmen

Pol

Kemner

et al. 2004

J Autism Dev Disord

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“…The strongest claims for a highly localized structural abnormality are those that relate to the involvement of the cerebellar vermis. Courchesne et al, (1987) reported hypoplasia of the posterior cerebellar vermis in an MRI study of a high functioning autistic individual. Subsequently 18 autistic individuals and a group of normal controls were examined; a significant reduction in the size of cerebellar vermal lobules VI-VII was found in the autistic group, but no difference in the size of vermal lobules I-V (Courchesne et al, 1988).…”

Section: Neuroimaging Studiesmentioning

confidence: 98%

Autism: Towards an Integration of Clinical, Genetic, Neuropsychological, and Neurobiological Perspectives

Bailey

Phillips

Rutter

1996

Child Psychology Psychiatry

680

359

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Autism constitutes one of the best validated child psychiatric disorders. Empirical research has succeeded in delineating the key clinical phenomena, in demonstrating strong genetic influences on the underlying liability, and in identifying basic cognitive deficits. A range of neurobiological abnormalities has also been found, although the replicability of specific findings has not been high. An understanding of the causal processes leading to autism, and accounting for the marked variability in its manifestations, requires an integration across these different levels of enquiry. Although this is not yet possible, a partial integration provides a useful strategy for identifying key research questions, the limitations of existing hypotheses, and future research directions that are likely to prove fruitful. The research findings for each research level are critically reviewed in order to consider how to move towards an integration across levels.

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“…The hypothesis that autism is associated with neuropathological changes was explored in the first reports published between 1980 and 1993 [7, 21, 22, 27, 42, 50, 51, 82, 90]. Since then, implementation of broader diagnostic terms such as Autism Spectrum Disorder (ASD), examination of larger cohorts, applications of stereology, and functional and structural magnetic resonance imaging (MRI) have resulted in the detection of several major types of pathology, most likely contributing to the clinical phenotype.…”

Section: Introductionmentioning

confidence: 99%

The neuropathology of autism: defects of neurogenesis and neuronal migration, and dysplastic changes

et al. 2010

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Autism is characterized by a broad spectrum of clinical manifestations including qualitative impairments in social interactions and communication, and repetitive and stereotyped patterns of behavior. Abnormal acceleration of brain growth in early childhood, signs of slower growth of neurons, and minicolumn developmental abnormalities suggest multiregional alterations. The aim of this study was to detect the patterns of focal qualitative developmental defects and to identify brain regions that are prone to developmental alterations in autism. Formalin-fixed brain hemispheres of 13 autistic (4–60 years of age) and 14 age-matched control subjects were embedded in celloidin and cut into 200-μm-thick coronal sections, which were stained with cresyl violet and used for neuropathological evaluation. Thickening of the subependymal cell layer in two brains and subependymal nodular dysplasia in one brain is indicative of active neurogenesis in two autistic children. Subcortical, periventricular, hippocampal and cerebellar heterotopias detected in the brains of four autistic subjects (31%) reflect abnormal neuronal migration. Multifocal cerebral dysplasia resulted in local distortion of the cytoarchitecture of the neocortex in four brains (31%), of the entorhinal cortex in two brains (15%), of the cornu Ammonis in four brains and of the dentate gyrus in two brains. Cerebellar flocculonodular dysplasia detected in six subjects (46%), focal dysplasia in the vermis in one case, and hypoplasia in one subject indicate local failure of cerebellar development in 62% of autistic subjects. Detection of flocculonodular dysplasia in only one control subject and of a broad spectrum of focal qualitative neuropathological developmental changes in 12 of 13 examined brains of autistic subjects (92%) reflects multiregional dysregulation of neurogenesis, neuronal migration and maturation in autism, which may contribute to the heterogeneity of the clinical phenotype.

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Abnormal Neuroanatomy in a Nonretarded Person With Autism

Cited by 144 publications

References 34 publications

Larger Brains in Medication Naive High-Functioning Subjects with Pervasive Developmental Disorder

Larger Brains in Medication Naive High-Functioning Subjects with Pervasive Developmental Disorder

Autism: Towards an Integration of Clinical, Genetic, Neuropsychological, and Neurobiological Perspectives

The neuropathology of autism: defects of neurogenesis and neuronal migration, and dysplastic changes

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