Cortical auditory system maturational abnormalities in children with autism disorder: an MEG investigation

Gage, Nicole M.; Siegel, Bryna; Roberts, Timothy P.L.

doi:10.1016/s0165-3806(03)00172-x

Cited by 117 publications

(114 citation statements)

References 38 publications

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“…As such, distinguishing between different frequencies within this range is of great importance for communication. In preliminary studies examining ASD, whereas the general form of the M100 latency response as a function of tone frequency was intact in children with ASD and typically developing controls (conforming to a 1/frequency model), the dynamic range in children with ASD (the latency difference between M100 responses to nominal high, 1kHz, and low, 100Hz, frequency stimuli) was markedly reduced in the right hemisphere of children with autism, showing only a 15-20 ms prolongation at low frequencies (100Hz) compared to high frequencies (1kHz) (Gage et al, 2003a). These observations led to the hypothesis that early detection systems and frequency analysis problems occurring at ~100ms may be impaired in children with autism, perhaps leading to imprecisely encoded auditory representations, and degraded "processed" data being input to subsequent neural systems.…”

Section: Frequency Encoding In the Brain Of Children With Autismmentioning

confidence: 74%

Electrophysiological signatures: Magnetoencephalographic studies of the neural correlates of language impairment in autism spectrum disorders

Roberts

Schmidt

Egeth

et al. 2008

International Journal of Psychophysiology

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While magnetoencephalography (MEG) is of increasing utility in the assessment of pediatric patients with seizure disorders, this indication reflects only a part of the clinical potential of the technology. Beyond epilepsy, a broad range of developmental psychiatric disorders require the combined offerings of spatial and temporal resolution, along with direct sensitivity to neural electrical activity, that are offered by MEG. This article reviews the application of MEG in the study of auditory processing as an aspect of language impairment in children. Potential application is elaborated in the clinical case of autism spectrum disorders, a devastating disorder with prevalence of 1 in 150, poorly served by alternative imaging modalities. MEG offers both spatial and temporal insights, tentatively described as "electrophysiological signatures". Results demonstrate the sensitivity of MEG for detection of abnormalities of auditory processing in ASD and their clinical correlates. These findings offer promise for the comprehensive assessment of developmental neuropsychiatric disorders such as autism, but also suggest avenues for the development of MEG technology to adequately meet the needs of such populations, as well as providing conduits to basic sciences including neurobiology and genetics.

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Section: Frequency Encoding In the Brain Of Children With Autismmentioning

confidence: 74%

Electrophysiological signatures: Magnetoencephalographic studies of the neural correlates of language impairment in autism spectrum disorders

Roberts

Schmidt

Egeth

et al. 2008

International Journal of Psychophysiology

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“…Levitt and colleagues found altered cortical sulcal maps in children with autism [77]. Such changes in the architecture of important cortical processing areas could underlie the functional deficits in the development of cortical sound processing [51], visual-motor maps [88] and face recognition [42,94] that are observed in autism.…”

Section: Discussionmentioning

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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“…Moreover, numerous studies show structural alterations in the cerebral cortex of children with autism (Bailey et al, 1998;Casanova et al, 2002;Herbert et al, 2002;Levitt et al, 2003). Such changes in the size and architecture of important cortical processing areas may underlie functional deficits in the development of cortical sound processing (Gage et al, 2003), visuo-motor maps (Mueller et al, 2003) and face recognition Dawson et al, 2002) that are observed in autism. Clearly, stereological studies will have to confirm that the width changes we have measured are truly representative of volume changes and they will have to ascertain the relative participation of white and gray matter areas in any volume change.…”

Section: Neonatal Serotonin Depletions As An Animal Model For Autismmentioning

confidence: 99%

Neonatal serotonin depletion alters behavioral responses to spatial change and novelty

et al. 2007

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Multiple brain disorders that show serotonergic imbalances have a developmental onset. Experimental models indicate a role for serotonin as a morphogen in brain development. To selectively study the effects of serotonin depletions on cortical structural development and subsequent behavior, we developed a mouse model in which a serotonin neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), is injected into the medial forebrain bundle (mfb) on the day of birth. Littermates with saline injections into the mfb and age matched mice served as controls. This study characterized the extent and duration of serotonergic denervation after the selective neonatal lesion and investigated effects on exploratory behavior, spatial learning and anxiety in mice of both sexes. We report significant decreases in the serotonergic (5-HT) innervation to cortex and hippocampus, but not to subcortical forebrain structures in 5,7-DHT-lesioned mice. The depletion of 5-HT fibers in cortical areas was long lasting in lesioned mice but autoradiographic binding to high affinity 5-HT transporters was only transiently reduced. Male but not female lesioned mice reduced their exploration significantly in response to spatial rearrangement and object novelty, suggesting increased anxiety in response to change but normal spatial cognition. Our data show that developmental disruptions in the serotonergic innervation of cortex and hippocampus are sufficient to induce permanent, sex specific, behavioral alterations. These results may have significant implications for understanding brain disorders presenting with cortical morphogenetic abnormalities and altered serotonin neurotransmission, such as autism, schizophrenia and affective disorders.

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Cortical auditory system maturational abnormalities in children with autism disorder: an MEG investigation

Cited by 117 publications

References 38 publications

Electrophysiological signatures: Magnetoencephalographic studies of the neural correlates of language impairment in autism spectrum disorders

Electrophysiological signatures: Magnetoencephalographic studies of the neural correlates of language impairment in autism spectrum disorders

Modeling early cortical serotonergic deficits in autism

Neonatal serotonin depletion alters behavioral responses to spatial change and novelty

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