Background: Recent research has implicated impaired neural synchrony in autistic disorder (AD) as a key mechanism underlying reduced abilities to integrate sensory information into coherent representations. Speech processing and language acquisition rely critically on the exquisite temporal resolution of the auditory system. In healthy adults, latency of the M100 as detected by MEG, is closely coupled in time (<20ms) in left (LH) and right hemispheres (RH), with LH latency typically peaking slightly later than RH. Although the neural bases remain unknown, it is observed in response to both speech and non-speech sounds. Far less is known about the temporal coupling of M100 in LH and RH in typical development and language disorders, such as autism.

Objectives: To assess neural synchrony in cortical processing of natural speech tokens in children with AD.

Methods: We measured M100 latency in typically developing children (TD, N=9), children with AD (N=15), and their unaffected siblings (SIB, N=8) in response to natural speech tokens: consonant-vowel (CVs) syllables that differ in distinctive features: place of articulation, voice onset time or both. Difference in LH-RH M100 time-to-peak (offset) was examined by computing absolute M100 latency differences and by calculating a laterality index (LI) ([2(L-R)/(L+R)].

Results: TD mean absolute offsets ranged 0-46ms. AD mean absolute offsets ranged 0-98ms. SIB: mean absolute offsets ranged 0-53ms. Greater variability is seen in offsets for AD compared to TD and SIB. SIB have greater offset than TD. TD and SIB LIs were leftward for voiced CVs and rightward for unvoiced. AD LIs were leftward for all conditions.

Conclusions: TD hemisphere asymmetries are greater than adults and may reflect slow-to-mature cortical processes. Greater asymmetries in children with AD provide evidence for poor neural synchrony in cortical processes underlying speech perception. Unaffected siblings show greater hemisphere asymmetries than TD, but smaller than their AD siblings.