Accelerated maturation of white matter in young children with autism: A high b value DWI study

Bashat, Dafna Ben; Kronfeld-Duenias, Vered; Zachor, Ditza A.; Ekstein, Perla; Hendler, Talma; Tarrasch, Ricardo; Even, Ariela; Levy, Yonata; Ben-Sira, Liat

doi:10.1016/j.neuroimage.2007.04.060

Cited by 266 publications

(261 citation statements)

References 41 publications

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“…8 Less pruning, if present in our children with prenatal methamphetamine exposure, also could lead to higher cell density and restriction of water movement, and lower ADC, without specifically affecting directionality or FA.…”

Section: Thalamus (E) Globus Pallidus (F) Putamen (G) Caudate (H)mentioning

confidence: 89%

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Lower diffusion in white matter of children with prenatal methamphetamine exposure

Cloak

Ernst²,

Fujii³

et al. 2009

Neurology

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Section: Thalamus (E) Globus Pallidus (F) Putamen (G) Caudate (H)mentioning

confidence: 89%

“…Normal brain development shows the greatest changes in FA and diffusivity during the first 5 years of life. 7,8 DTI may also differentiate between stages of brain maturation. 9 In adult methamphetamine users, DTI demonstrated lower FA in the frontal white matter (WM).…”

mentioning

confidence: 99%

Lower diffusion in white matter of children with prenatal methamphetamine exposure

Cloak

Ernst²,

Fujii³

et al. 2009

Neurology

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“…Reports have been published revealing reduced long-range, distant brain connectivity during both task-specific (Besag 2004;Koshino et al 2005Koshino et al , 2008Kana et al 2006;Just et al 2007) and restingstate paradigms Weng et al 2010). Likewise, a number of studies have shown reduced short-range, local connectivity (Besag 2004;Koshino et al 2005Koshino et al , 2008Just et al 2007;Kana et al 2011). Results from yet other studies have shown increased connectivity, both long range (Ben Bashat et al 2007;Cheng et al 2010;Supekar et al 2013) and short range (Weng et al 2010;Anderson et al 2011;Keown et al 2013;Khan et al 2013;Lewis et al 2013). …”

Section: Aberrant Connectivity In Autismmentioning

confidence: 99%

Epilepsy and Autism

Buckley

Holmes

2016

Cold Spring Harb Perspect Med

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Epilepsy and autistic spectrum disorder frequently coexist in the same individual. Electroencephalogram (EEG) epileptiform activity is also present at a substantially higher rate in children with autism than normally developing children. As with epilepsy, there are a multitude of genetic and environmental factors that can result in autistic spectrum disorder. There is growing consensus from both animal and clinical studies that autism is a disorder of aberrant connectivity. As measured with functional magnetic resonance imaging (MRI) and EEG, the brain in autistic spectrum disorder may be under-or overconnected or have a mixture of over-and underconnectivity. In the case of comorbid epilepsy and autism, an imbalance of the excitatory/inhibitory (E/I) ratio in selected regions of the brain may drive overconnectivity. Understanding the mechanism by which altered connectivity in individuals with comorbid epilepsy and autistic spectrum disorder results in the behaviors specific to the autistic spectrum disorder remains a challenge.

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“…Adolescents with COS are characterized by a striking nonlinear, progressive acceleration of the normal gray matter and volume decrease in cortical regions that levels off in adulthood (22). In autism, there is an early left hemispheric overgrowth of gray and white matter at young toddler age with conflicting findings of either arrested growth or remaining brain enlargement in adolescence and adulthood (23). The findings of delayed structural brain maturation seem, thus far, to be specific to ADHD and may be an important neuroanatomic trait.…”

Section: Implications Clinical Relevance and Future Directionsmentioning

confidence: 99%

Neuro-anatomic evidence for the maturational delay hypothesis of ADHD

Rubia

2007

Proc. Natl. Acad. Sci. U.S.A.

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A ttention deficit hyperactivity disorder (ADHD) has been hypothesized to be related to a delay rather than a deviance of normal brain development before it was first defined by the DSM-III (1). The hypothesis was initially based on the behavioral observation that children with ADHD behave like younger children who are naturally more active, more impulsive, and have a shorter attention span than older children. This is well expressed in the definition of the disorder in the DSM-IV, where ADHD is characterized by an age-inappropriate display of inattention, hyperactivity, and impulsiveness. The behavioral observation is further supported by the cognitive profile of ADHD children: They show deficits in late developing higher cognitive functions of inhibitory selfcontrol, attention, and temporal foresight (2, 3). The fact that ADHD symptoms tend to improve with age and up to 80% of children (depending on the follow-up length and definition of persistence) grow out of ADHD in adulthood (4) further supports the theory of a maturational lag that eventually normalizes in a considerable proportion of children. Indirect neurobiological support comes from cross-sectional structural imaging studies finding reduced size in cortico-striatal brain regions that are known to develop late in adolescence (5) and functional imaging studies showing reduced brain activation in ADHD compared with their age-matched peers in precisely those brain areas whose functions develop progressively with age between childhood and adulthood (6-10). Crosssectional studies, however, are confounded by cohort effects; direct testing of the maturational delay hypothesis requires longitudinal imaging studies that map the developmental trajectories of brain maturation in healthy and ADHD children. In a recent issue of PNAS, Shaw et al. (11) study largely longitudinal data to provide direct neurobiological evidence for the maturational delay hypothesis of ADHD. ADHD Is a Delay of Normal Brain MaturationPrevious mixed longitudinal and crosssectional structural MRI studies of the same research group in Ͼ150 ADHD children scanned repeatedly between 5 and 20 years showed that ADHD children are characterized by a nonprogressive reduction in gray and white matter (2) and cortical thickness in cortical and cerebellar brain regions (11). Developmental growth curves in almost all cortical regions in ADHD children were lower but still parallel to those of controls. These findings can be interpreted as a maturational delay, because they suggest that ADHD children are ''limping behind'' normal development in a nonprogressive fashion. However, the relatively gross volumetric analyses of the cortical lobes in the first study (2) and the relative lack of power to investigate nonlinear changes in the second study (12) prevented the authors from detecting differences in developmental peaks within cortical brain areas. Shaw et al. (11) measured cortical thickness that can demonstrate considerable variability in timing of cortical maturation within each lobe in sufficientl...

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Accelerated maturation of white matter in young children with autism: A high b value DWI study

Cited by 266 publications

References 41 publications

Lower diffusion in white matter of children with prenatal methamphetamine exposure

Lower diffusion in white matter of children with prenatal methamphetamine exposure

Epilepsy and Autism

Neuro-anatomic evidence for the maturational delay hypothesis of ADHD

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