Cerebral Lobes in Autism: Early Hyperplasia and Abnormal Age Effects

Carper, Ruth A.; Moses, Pamela; Tigue, Zachary; Courchesne, Eric

doi:10.1006/nimg.2002.1099

Cited by 504 publications

(459 citation statements)

References 67 publications

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“…As described previously, children with autism have significantly increased cortical volumes at 2 to 4 years of age, as the result of an early, exuberant brain overgrowth [20,38]. Cortical volume normalizes with increasing age into adulthood [97] and, depending on the report, may be smaller in later life [102].…”

Section: Discussionmentioning

confidence: 56%

“…The findings of early postnatal brain overgrowth in autism followed by an abrupt cessation of growth in childhood, were recently confirmed in a meta-analysis of all eligible reports examining head circumference, magnetic resonance imaging (MRI), or postmortem brain weights from autism cases [97]. Initial MRI evaluation indicated that the increased brain volume in children with autism is the result of increased cerebral cortical gray matter and cerebral and cerebellar white matter [20,38]. However, more recent studies have demonstrated consistent increases in white matter volumes in children with autism [6,[56][57][58], which may be more pertinent to the key deficits in autism involving processing of complex social, sensory and language information.…”

Section: Introductionmentioning

confidence: 88%

“…-stereotypical behaviors, impaired verbal and nonverbal communication and blunted social interaction) are accompanied by structural and functional changes in cortex, cerebellum and amygdala [3,4,7,8,[19][20][21][22]37,38,49,55,67,101,125]. Structural and functional changes apparent in early childhood suggest that autism is a disorder of brain development [4,19,20,[37][38][39]111].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Modeling early cortical serotonergic deficits in autism

Boylan

Blue

Höhmann

2007

Behavioural Brain Research

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Autism is a developmental brain disorder characterized by deficits in social interaction, language and behavior. Brain imaging studies demonstrate increased cerebral cortical volumes and micro-and macroscopic neuroanatomic changes in children with this disorder. Alterations in forebrain serotonergic function may underlie the neuroanatomic and behavioral features of autism. Serotonin is involved in neuronal growth and plasticity and these actions are likely mediated via serotonergic and glutamatergic receptors. Few animal models of autism have been described that replicate both etiology and pathophysiology. We report here on a selective serotonin (5-HT) depletion model of this disorder in neonatal mice that mimics neurochemical and structural changes in cortex and, in addition, displays a behavioral phenotype consistent with autism. Newborn male and female mice were depleted of forebrain 5-HT with injections of the serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), into the bilateral medial forebrain bundle (mfb). Behavioral testing of these animals as adults revealed alterations in social, sensory and stereotypic behaviors. Lesioned mice showed significantly increased cortical width. Serotonin immunocytochemistry showed a dramatic long-lasting depletion of 5-HT containing fibers in cerebral cortex until postnatal day (PND) 60. Autoradiographic binding to high affinity 5-HT transporters was significantly but transiently reduced in cerebral cortex of 5,7-DHT-depleted mice. AMPA glutamate receptor binding was decreased at PND 15. We hypothesize that increased cerebral cortical volume and sensorimotor, cognitive and social deficits observed in both 5-HT-depleted animals and in individuals with autism, may be the result of deficiencies in timely axonal pruning to key cerebral cortical areas.

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Section: Discussionmentioning

confidence: 56%

Section: Introductionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

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Modeling early cortical serotonergic deficits in autism

Boylan

Blue

Höhmann

2007

Behavioural Brain Research

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“…It is interesting to note that Piven et al (1996) found increased volume of the parietal, temporal, and posterior lobes, but not the frontal lobes in autism compared to normal control. Carper et al (2002) did not find statistically significant frontal, temporal, parietal, and occipital white matter volume differences between the groups in age range 7.5 -11.5 years; however, their regression analysis showed that the predicted white matter volume at age 12 is substantially lower in the autistic group. The orbital frontal cortex projects through the rostrum while occipital and inferior temporal cortex project through the splenium (Hardan et al, 2000).…”

Section: Discussionmentioning

confidence: 80%

Less white matter concentration in autism: 2D voxel-based morphometry

Chung¹,

Dalton²,

Alexander³

et al. 2004

NeuroImage

143

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Autism is a neurodevelopmental disorder affecting behavioral and social cognition, but there is little understanding about the link between the functional deficit and its underlying neuroanatomy. We applied a 2D version of voxel-based morphometry (VBM) in differentiating the white matter concentration of the corpus callosum for the group of 16 high functioning autistic and 12 normal subjects. Using the white matter density as an index for neural connectivity, autism is shown to exhibit less white matter concentration in the region of the genu, rostrum, and splenium removing the effect of age based on the general linear model (GLM) framework. Further, it is shown that the less white matter concentration in the corpus callosum in autism is due to hypoplasia rather than atrophy. D

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“…While most human sutures do not close until adulthood, the metopic, or frontal suture, closes by approximately age two (Cohen, 1993). Several authors have reported that the regions with the most abnormally increased volume in autism are frontal gray and white matter (Carper and Courchesne, 2005;Carper et al, 2002;Herbert et al, 2004). The regional reduction in the volume of the frontal horn of the left ventricle (and the strong trend to a regional reduction in the right frontal ventricular volume) could therefore be a reflection of excessive frontal growth.…”

Section: Discussionmentioning

confidence: 99%

Three-dimensional mapping of the lateral ventricles in autism

Vidal¹,

Nicolson

Boire

et al. 2008

Psychiatry Research: Neuroimaging

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In this study, a computational mapping technique was used to examine the three-dimensional profile of the lateral ventricles in autism. T1-weighted three-dimensional magnetic resonance images of the brain were acquired from 20 males with autism (age: 10.1 ± 3.5 years) and 22 male control subjects (age: 10.7 ± 2.5 years). The lateral ventricles were delineated manually and ventricular volumes were compared between the two groups. Ventricular traces were also converted into statistical threedimensional maps, based on anatomical surface meshes. These maps were used to visualize regional morphological differences in the thickness of the lateral ventricles between patients and controls. Although ventricular volumes measured using traditional methods did not differ significantly between groups, statistical surface maps revealed subtle, highly localized reductions in ventricular size in patients with autism in the left frontal and occipital horns. These localized reductions in the lateral ventricles may result from exaggerated brain growth early in life.

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Cerebral Lobes in Autism: Early Hyperplasia and Abnormal Age Effects

Cited by 504 publications

References 67 publications

Modeling early cortical serotonergic deficits in autism

Modeling early cortical serotonergic deficits in autism

Less white matter concentration in autism: 2D voxel-based morphometry

Three-dimensional mapping of the lateral ventricles in autism

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