Identifying the Origins of Postural Control Deficits in Autism Spectrum Disorders: Sensory Acuity Vs. Sensory Integration

Poster Presentation
Friday, May 11, 2018: 5:30 PM-7:00 PM
Hall Grote Zaal (de Doelen ICC Rotterdam)
M. Doumas1, R. Knox2, C. Craig3 and C. O'Brien2, (1)School of Psychology, Queen's University Belfast, Belfast, United Kingdom, (2)Queen's University Belfast, Belfast, United Kingdom, (3)Manchester Metropolitan University, Manchester, United Kingdom
Background: Individuals with Autism Spectrum Disorders (ASD) experience the world differently compared with neurotypical individuals. ASD is characterised by deficits in social interaction and communication, but also in sensory processing and motor control. One of the key aspects of movement affected by ASD is postural control. Postural control deficits in ASD are well established, however, the underlying mechanisms of these deficits are not well understood. Recent studies suggest that the increased postural instability observed in individuals with ASD is most evident when one or more of the sensory channels (visual, vestibular and proprioceptive) involved in this task is compromised. Thus, this impairment is likely to be either due to impaired acuity of information from these channels, due to impaired sensory integration processes, or both.

Objectives: The main objective of this study was to assess the contribution of sensory acuity and sensory integration to the postural control deficits of individuals with ASD. We hypothesized that these deficits will be due to sensory integration rather than sensory acuity.

Methods: Fifteen high functioning (IQ>80) young adults with ASD (2 female, age range 18-35 years) and 15 age- and gender-matched neurotypical adults participated in our study. They first performed an ankle joint-position matching task measuring proprioceptive acuity. Then, they performed a postural control task, without vision, thus involving only proprioceptive and vestibular information. Participants were asked to stand on a fixed surface (baseline, 2 minutes), immediately followed by standing on a sway referenced surface (adaptation, 3 minutes) which induced inaccurate proprioceptive information about body sway, and then again on a fixed surface (reintegration, 3 minutes).

Results: Participants with ASD and neurotypical controls were not different in absolute and variable error in the joint position-matching task. In the balance task, no group differences in AP (Anterior-Posterior) and ML (Medio-Lateral) path length were shown during baseline. Subsequently, when sway referencing was introduced AP and ML path length increased in both groups as expected. However, over the course of the 3 minutes of adaptation to this environment, neurotypical participants were able to reduce sway especially in the AP direction over time through adaptation. In contrast, participants with ASD did not exhibit this ability to adapt to the sway referenced environment by reducing sway over time, reflecting an inability to reweight proprioceptive and vestibular information during postural control. Finally, when the fixed surface was restored both groups were able to return to their baseline levels of sway at the same rate.

Conclusions: These results confirm our hypothesis that the postural control deficit observed in individuals with ASD is primarily due to central, sensory integration deficits rather than peripheral, sensory noise. Future research is needed to identify ways to moderate this deficit in order to improve motor skill performance and quality of life in children and adults with ASD.