MEG INVESTIGATIONS OF NEURAL SYNCHRONY IN AUDITORY LANGUAGE CORTEX IN CHILDREN WITH AUTISTIC DISORDER, THEIR UNAFFECTED SIBLINGS, AND TYPICALLY DEVELOPING CONTROLS

Background: we have provided evidence for impaired feature extraction processes in auditory language cortex in children with autistic disorder (AD) vs. typically developing (TD) controls (Gage et al., 2003).

Objectives: to assess temporal acuity within auditory language cortex and neural synchrony across hemispheres to determine if feature extraction impairments were due to reduced neural synchrony within- and across-hemispheres in children with AD.

Methods: in healthy adults, M100 latency is prolonged in a near-linear manner by brief discontinuities (silent gaps 0-20 ms) at the onset of sounds (Gage et al., 2006), demonstrating the high temporal resolution of auditory language cortex. We used identical stimuli and measured M100 latency to 1kHz tones with gaps (0, 5, 10, 20ms) in 17 (15 male, 7-14 yrs) children with AD, and 17 (15 male, 7-14 yrs) controls. Within the control group, 8 (6 male) were unaffected siblings (SIB) of the AD group and 9 (all male) were unrelated TD controls.

Results: M100 dynamic range (DR) was calculated (20-gap – 0-gap) to assess magnitude of within-hemisphere modulation by gaps, a measure of temporal acuity. Laterality index (LI, (2*(L-R)/(L+R)) was calculated for the 0-gap and 20-gap conditions to assess the magnitude of between-hemispheres temporal offsets, a measure of neural synchrony. DR - AD: LH 13.8ms, RH 7.8ms; SIB: LH 25.1, RH 26.6; TD LH 18.5, RH 30.4. LI - AD: 0-gap 0.111, 20-gap 0.129; SIB: 0-gap 0.079, 20-gap 0.081; TD: 0-gap 0.064, 20-gap 0.089.

Conclusions: Children with AD evidenced reduced within-hemisphere temporal acuity to fine-grained features, particularly in RH, and increased between-hemisphere asynchrony vs. TD or SIB groups. Together these findings provide evidence for impairments in temporal resolution and neural synchrony within- and across-hemispheres in auditory language cortex for children with AD that are not present in their unaffected siblings or unrelated controls.