Effects of age on brain volume and head circumference in autism

Aylward, Elizabeth H.; Minshew, Nancy J.; Field, Katharine G.; Sparks, Bobbi F.; Singh, Namrata

doi:10.1212/wnl.59.2.175

Cited by 433 publications

(349 citation statements)

References 45 publications

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“…Age differences may partly reflect a particular neuro-developmental pattern in autism. Brain development in autism follows an abnormal pattern, with accelerated growth in early life (resulting in brain enlargement) and subsequent decrease in brain volume in later life, as a part of a maturation/normalization process (Aylward et al, 2002). Consequently, such a neurodevelopmental process could account for the fact that autism was found to be more frequent in younger (< 35) than in older patients.…”

Section: Discussionmentioning

confidence: 99%

Psychopathology in Adults with Autism and Intellectual Disability

Tsakanikos

Costello

Holt

et al. 2006

J Autism Dev Disord

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There have been few studies of psychopathology in adult with autism. This study examined psychiatric co-morbidity in 147 adults with intellectual disability (ID) and autism and 605 adults with ID but without autism. After controlling for the effects of gender, age, psychotropic medication and level of ID, people with autism and ID were no more likely to receive a psychiatric diagnosis than people with ID only. People with autism were less likely to receive a diagnosis of personality disorder. These findings cast doubts on the hypothesis that adults with ID and autism are more vulnerable to certain psychiatric disorders than non-autistic adults with ID.

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Section: Discussionmentioning

confidence: 99%

Psychopathology in Adults with Autism and Intellectual Disability

Tsakanikos

Costello

Holt

et al. 2006

J Autism Dev Disord

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“…-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%

“…Affected children are born with small to normal sized brains, but they then experience rapid and excessive brain growth within the first years of life resulting in increased cortical volume at 2 to 4 years of age [38,111]. This abnormal growth slows so that by late adolescence, brains are the same size as unaffected adults [3]. 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].…”

Section: Introductionmentioning

confidence: 99%

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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“…This heterogeneity is both longitudinal and cross-sectional. Longitudinally, especially given autism's nature as a developmental disorder, measurements can be expected to change over the course of maturation and aging (Aylward, Minshew, Field, Sparks, & Singh, 2002;Carper, Moses, Tigue, & Courchesne, 2002). [The inconsistency of recent findings on the size of the amygdala at various ages is a case in point (Baron-Cohen, Knickmeyer, & Belmonte, 2005).]…”

Section: The Problemmentioning

confidence: 99%

“…Derived measures can include segmented tissue volumes, landmarking and parcellation, structure volumes, and fibre maps in a set of standard subjects ("living phantoms") scanned at multiple sites. Validity of automated landmarking and parcellation could be established with reference to "gold standard" measures, many of which already exist as by-products of studies of specific cortical and subcortical structures in autism (Aylward et al, 2002;Carper et al, 2002). These standards can be refined in collaboration with an independent expert in neuroanatomy.…”

Section: Standards For Comparability Of Derived Datamentioning

confidence: 99%

Offering to Share: How to Put Heads Together in Autism Neuroimaging

Belmonte

Mazziotta

Minshew

et al. 2007

J Autism Dev Disord

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Data sharing in autism neuroimaging presents scientific, technical, and social obstacles. We outline the desiderata for a data-sharing scheme that combines imaging with other measures of phenotype and with genetics, defines requirements for comparability of derived data and NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript recommendations for raw data, outlines a core protocol including multispectral structural and diffusion-tensor imaging and optional extensions, provides for the collection of prospective, confound-free normative data, and extends sharing and collaborative development not only to data but to the analytical tools and methods applied to these data. A theme in these requirements is the need to preserve creative approaches and risk-taking within individual laboratories at the same time as common standards are provided for these laboratories to build on. KeywordsImaging; MRI; PET; Morphometry; Segmentation; Data sharing The ProblemTracing the behaviourally defined syndrome of autism to its neurobiological roots poses a difficulty since autism is heterogeneous in terms of its detailed symptom profiles (Ronald, Happé, & Plomin, 2005), genetic and environmental antecedents (Veenstra-Vanderweele, Christian, & Cook, 2004) and developmental mechanisms (Belmonte et al., 2004a). Because autism in this regard may be an amalgam of many unknown conditions, it seems a foregone conclusion that behaviourally ascertained groups of subjects contain large amounts of unmodelled variance, and that the relation between group size and statistical power is a steep one (Coon, 2006). This problem of sample size in the context of heterogeneous conditions is particularly acute in the domain of brain imaging, where costs are great and small samples are therefore more accepted and more usual. A solution seems clear in principle: the many small data sets collected by various investigators ought to be pooled into one large data set for analysis. Several obstacles, though, make such data sharing easier said than done. These obstacles are scientific, technical, and social-but not insurmountable.The scientific obstacles are matters of sample heterogeneity, which complicate the comparability of separately ascertained groups. This heterogeneity is both longitudinal and cross-sectional. Longitudinally, especially given autism's nature as a developmental disorder, measurements can be expected to change over the course of maturation and aging (Aylward, Minshew, Field, Sparks, & Singh, 2002;Carper, Moses, Tigue, & Courchesne, 2002). [The inconsistency of recent findings on the size of the amygdala at various ages is a case in point (Baron-Cohen, Knickmeyer, & Belmonte, 2005).] The consequent need to control and account for age particularly hampers retrospective efforts to combine separately ascertained samples. Cross-sectionally, autism's multiplicity of symptom profiles and neurobiological mechanisms makes it imperative to correlate imaging with other measures of potential endophenotypes, heightening the...

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Effects of age on brain volume and head circumference in autism

Cited by 433 publications

References 45 publications

Psychopathology in Adults with Autism and Intellectual Disability

Psychopathology in Adults with Autism and Intellectual Disability

Modeling early cortical serotonergic deficits in autism

Offering to Share: How to Put Heads Together in Autism Neuroimaging

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