2002
DOI: 10.1038/sj.mp.4001169
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Abnormal early brain development in autism

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Cited by 138 publications
(102 citation statements)
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“…As mentioned previously, VPA rats also show brain abnormalities resembling those found for autopsy and in brain-imaging studies of autistic patients (Bauman and Kemper, 1985, 1997Gaffney et al, 1988;Hashimoto et al, 1989Hashimoto et al, , 1992Hashimoto et al, , 1995Kemper and Bauman, 1993;Courchesne, 1994Courchesne, , 1997Courchesne, , 2002Rodier et al, 1996Rodier et al, , 1997Ingram et al, 2000). Therefore, VPA rodent model of autism appears to parallel both anatomical and functional pathology reported in autism and related neurodevelopmental disorders confirming validity of the model and its usefulness for further studies.…”
Section: Discussionsupporting
confidence: 51%
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“…As mentioned previously, VPA rats also show brain abnormalities resembling those found for autopsy and in brain-imaging studies of autistic patients (Bauman and Kemper, 1985, 1997Gaffney et al, 1988;Hashimoto et al, 1989Hashimoto et al, , 1992Hashimoto et al, , 1995Kemper and Bauman, 1993;Courchesne, 1994Courchesne, , 1997Courchesne, , 2002Rodier et al, 1996Rodier et al, , 1997Ingram et al, 2000). Therefore, VPA rodent model of autism appears to parallel both anatomical and functional pathology reported in autism and related neurodevelopmental disorders confirming validity of the model and its usefulness for further studies.…”
Section: Discussionsupporting
confidence: 51%
“…The 20-24th day of gestation is the time of neural tube closure and development of the first neurons, which form the motor nuclei of the cranial nerves. Histological, anatomical, and MRI studies of nonthalidomide autistic patients' brains confirm existence of very early developmental deficits in this disorder and indicate: (1) abnormalities of the cranial nerve nuclei, (2) hypoplasia of brainstem structures, (3) reduced volume of posterior parts of cerebellar vermis and hemispheres with a loss of Purkinje cells, and (4) injury to deep nuclei of the cerebellum (Bauman and Kemper, 1985, 1997Gaffney et al, 1988;Hashimoto et al, 1989Hashimoto et al, , 1992Hashimoto et al, , 1995Kemper and Bauman, 1993;Courchesne, 1994Courchesne, , 1997Courchesne, , 2002Rodier et al, 1996Rodier et al, , 1997. The absence of gliosis following neuron loss in the described structures suggests that the damage could have occurred only during very early stages of brain development (Sumi and Hager, 1968;Gilles, 1983).…”
Section: Introductionmentioning
confidence: 98%
“…Longitudinal studies using MRI volumetric and head circumference data point to the conclusion that autism involves transient postnatal macrencephaly [64]. Although nonstandardised measurements of head circumference must be viewed with some caution, the data currently available on newborns later diagnosed with autism or PDD-NOS suggest that head size at the time of birth is normal or perhaps even slightly smaller than normal [65].…”
Section: Anatomical Correlatesmentioning
confidence: 99%
“…Additionally, there is some evidence that the changes in neuronal organization in ASD are differentially expressed with age, marked by early life brain overgrowth including increased neuron number, followed by decreases in both structural volumes and neuron number as the brain ages. Courchesne (2002Courchesne ( , 2004 and Courchesne and colleagues (2003) identified growth abnormalities in frontal, cerebellar, and temporal structures that normally mediate the development of higher order social, emotional, speech, language, attention, and cognitive functions that are often abnormal in ASD. In other structures (e.g., occipital cortex), known to mediate functions that are either mildly or entirely unaffected in ASD patients, growth pathologies are milder or nonexistent (Courchesne et al 2005).…”
Section: Aberrant Connectivity In Autismmentioning
confidence: 99%