Abstract
Individuals with autism spectrum disorder (ASD) have severe difficulties in social interaction and communication, as well as restricted and/or stereotyped patterns of behavior. Previous studies have suggested that abnormal neural connectivity might be associated with higher information processing dysfunction involving social impairment. However, the white matter structure in ASD is poorly understood. To explore this, we conducted a voxel-based, whole-brain diffusion tensor imaging (DTI) analysis to determine fractional anisotropy (FA), λ1, λ2 and λ3 in high-functioning children with ASD compared with age-, gender-, and handedness-matched healthy control participants. We then investigated whether DTI parameters were associated with behaviorally measured social function. We found that FA and λ1 were significantly lower in the ASD group than in the control group in the white matter around left dorsolateral prefrontal cortex (DLPFC), posterior superior temporal sulcus/temporo-parietal junction, right temporal pole, amygdala, superior longitudinal fasciculus, occipitofrontal fasciculus, mid- and left anterior corpus callosum, and mid- and right anterior cingulate cortex. The FA value in the left DLPFC was negatively correlated with the degree of social impairment in children with ASD. Higher λ1 values were observed in the cerebellar vermis lobules in the ASD group. The white matter alterations in children with ASD were around cortical regions that play important roles in social cognition and information integration. These DTI results and their relationship to social impairment add to evidence of cerebral and cerebellar white matter structural abnormalities in ASD.
| Original language | English |
|---|---|
| Pages (from-to) | 141-149 |
| Number of pages | 9 |
| Journal | Brain Research |
| Volume | 1362 |
| DOIs | |
| Publication status | Published - Nov 29 2010 |
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All Science Journal Classification (ASJC) codes
- Neuroscience(all)
- Molecular Biology
- Clinical Neurology
- Developmental Biology
Cite this
Altered white matter fractional anisotropy and social impairment in children with autism spectrum disorder. / Noriuchi, Madoka; Kikuchi, Yoshiaki; Yoshiura, Takashi; Kira, Ryutaro; Shigeto, Hiroshi; Hara, Toshiro; Tobimatsu, Shozo; Kamio, Yoko.
In: Brain Research, Vol. 1362, 29.11.2010, p. 141-149.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Altered white matter fractional anisotropy and social impairment in children with autism spectrum disorder
AU - Noriuchi, Madoka
AU - Kikuchi, Yoshiaki
AU - Yoshiura, Takashi
AU - Kira, Ryutaro
AU - Shigeto, Hiroshi
AU - Hara, Toshiro
AU - Tobimatsu, Shozo
AU - Kamio, Yoko
PY - 2010/11/29
Y1 - 2010/11/29
N2 - Individuals with autism spectrum disorder (ASD) have severe difficulties in social interaction and communication, as well as restricted and/or stereotyped patterns of behavior. Previous studies have suggested that abnormal neural connectivity might be associated with higher information processing dysfunction involving social impairment. However, the white matter structure in ASD is poorly understood. To explore this, we conducted a voxel-based, whole-brain diffusion tensor imaging (DTI) analysis to determine fractional anisotropy (FA), λ1, λ2 and λ3 in high-functioning children with ASD compared with age-, gender-, and handedness-matched healthy control participants. We then investigated whether DTI parameters were associated with behaviorally measured social function. We found that FA and λ1 were significantly lower in the ASD group than in the control group in the white matter around left dorsolateral prefrontal cortex (DLPFC), posterior superior temporal sulcus/temporo-parietal junction, right temporal pole, amygdala, superior longitudinal fasciculus, occipitofrontal fasciculus, mid- and left anterior corpus callosum, and mid- and right anterior cingulate cortex. The FA value in the left DLPFC was negatively correlated with the degree of social impairment in children with ASD. Higher λ1 values were observed in the cerebellar vermis lobules in the ASD group. The white matter alterations in children with ASD were around cortical regions that play important roles in social cognition and information integration. These DTI results and their relationship to social impairment add to evidence of cerebral and cerebellar white matter structural abnormalities in ASD.
AB - Individuals with autism spectrum disorder (ASD) have severe difficulties in social interaction and communication, as well as restricted and/or stereotyped patterns of behavior. Previous studies have suggested that abnormal neural connectivity might be associated with higher information processing dysfunction involving social impairment. However, the white matter structure in ASD is poorly understood. To explore this, we conducted a voxel-based, whole-brain diffusion tensor imaging (DTI) analysis to determine fractional anisotropy (FA), λ1, λ2 and λ3 in high-functioning children with ASD compared with age-, gender-, and handedness-matched healthy control participants. We then investigated whether DTI parameters were associated with behaviorally measured social function. We found that FA and λ1 were significantly lower in the ASD group than in the control group in the white matter around left dorsolateral prefrontal cortex (DLPFC), posterior superior temporal sulcus/temporo-parietal junction, right temporal pole, amygdala, superior longitudinal fasciculus, occipitofrontal fasciculus, mid- and left anterior corpus callosum, and mid- and right anterior cingulate cortex. The FA value in the left DLPFC was negatively correlated with the degree of social impairment in children with ASD. Higher λ1 values were observed in the cerebellar vermis lobules in the ASD group. The white matter alterations in children with ASD were around cortical regions that play important roles in social cognition and information integration. These DTI results and their relationship to social impairment add to evidence of cerebral and cerebellar white matter structural abnormalities in ASD.
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UR - http://www.scopus.com/inward/citedby.url?scp=78149360411&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2010.09.051
DO - 10.1016/j.brainres.2010.09.051
M3 - Article
C2 - 20858472
AN - SCOPUS:78149360411
VL - 1362
SP - 141
EP - 149
JO - Brain Research
JF - Brain Research
SN - 0006-8993
ER -