The course and prognostic capability of motor difficulties in infants showing early signs of autism.

Abstract

Delays within the motor domain are often overlooked as an early surveillance marker for autism. The present study evaluated motor difficulties and its potential as an early predictive marker for later autism likelihood in a cohort of infants (N=96) showing early behavioral signs of autism aged 9-14 months. The motor domain was evaluated using the motor subscales of the Mullen Scales of Early Learning at baseline, and at a 6-month follow-up. The Autism Diagnostic Observation Schedule - Toddler Module (ADOS-T) was completed at follow-up as a measure of autism likelihood. Motor difficulties were common at baseline, with 63/96 (65.6%) infants scoring very low or below average in the gross motor domain and 29/96 (30.2%) in the fine motor domain. At follow-up, gross motor difficulties had resolved for many, with 23/63 (36.5%) infants maintaining these difficulties. Fine motor difficulties resolved in fewer infants, with 20/29 (69.0%) continuing to present with fine motor delays at follow-up. Adjusted linear regression models suggested that fine motor scores at baseline (β=-0.12, SE=0.04) and follow-up (β=-0.17, SE=0.05) were associated with higher ADOS-T scores; with difficulties across both timepoints (β=5.60, SE=1.35) the strongest (largest in magnitude) association with ADOS-T scores of the predictors examined. Motor difficulties are prominent in children displaying emerging signs of autism, with persistent fine motor difficulties predictive of the developing autism phenotype. The findings indicate the potential clinical value of including evaluation of motor skills within early autism surveillance measures. LAY SUMMARY: This prospective study evaluated motor development over a 6-month period in infants showing early behavioral signs of autism. Atypical motor development was a common feature of infants showing early signs of autism and persistent fine motor difficulties were predictive of the emerging autism phenotype.