Is motor dysfunction core to autism spectrum disorder?

Authors

  • NICOLE RINEHART,

    1.  Centre for Developmental Psychiatry and Psychology, School of Psychology and Psychiatry, Monash University, Melbourne, Victoria, Australia
    Search for more papers by this author
  • JENNIFER McGINLEY

    1.  Murdoch Children’s Research Institute, Royal Children's Hospital, Parkville, Victoria, Australia
    2.  The School of Physiotherapy, The University of Melbourne, Victoria, Australia.
    Search for more papers by this author

  • This article is a commentary on Van Waelvelde et al., pp e174e178 of this issue.

There is a well-established link between early motor developmental trajectories and psychosocial outcomes in childhood. This is well-highlighted in children with autism spectrum disorders (ASD), where motor skill deficits have an impact on schooling, socialization, and contribute to communication deficits.1 Van Waelvelde et al.’s2 study has documented the persistent nature of these motor impairments which may present additional challenges to the quality of life of children with ASD. The persistent nature of these motor impairments is of great interest to the growing debate about whether motor symptoms may in fact be a biomarker, and indeed a core symptom of ASD. The most recent imaging evidence suggests cerebellar motor features may be specifically linked to ASD.3 Mostofsky et al. reported that children with ASD show less activation in the cerebellum (unconscious planned movements) with relatively more activation in the fronto-striatal region (conscious planned movements). This type of neuromotor signature may account for the significant and pervasive difficulties children with ASD experience on the Movement Assessment Battery for Children (MABC), where some of the tasks involve fast and automatic responses, e.g. catching and throwing a ball; such automatic responses are best achieved below the level of conscious awareness. In the absence of efficient cerebellar functions to achieve this less conscious motoric response, children with ASD may operate at a more conscious level which would place greater demands on the attentional and executive control centres of the brain, in particular, the fronto-striatal regions, which are themselves compromised in children with ASD.

A discussion of motor dysfunction in ASD is incomplete without mentioning the phenomenon of kinesia paradoxa.1 It has been commonly observed that when children with ASD become fixated on a motor task, e.g. computer games, running, rapidly responding to or engaging in a gross motor task, motor function can appear smooth and seamless. It may be that the thalamus, an area that is neuroanatomically anomalous in autism, and has major connections to both the cerebellum and fronto-striatal basal ganglia circuits, may play an important modulatory role in motor behaviour and underpin kinesia paradoxa.4 Further research is needed to investigate the contextual dependence on motor symptoms in children with ASD.

If motor anomalies in ASD are ‘core’ and not symptoms which children with ASD ‘grow out of’ in the way that children with primary attention-deficit–hyperactivity disorder (ADHD) symptoms may, then this has major implication for occupational and physical therapy interventions. Attention must therefore be directed at evaluation of the role of therapy for these motor disorders. A case in point is intervention for dysgraphia, a common difficulty which significantly interferes with academic functioning in children with ASD, and is often an entry point for occupational therapy intervention. If dysgraphia is underpinned by a fundamental disruption to cerebellar-fronto-striatal circuitry, and, like performance on the MABC, is stable over time in children with ASD, should interventions be targeted at improving hand-writing or working around the problem to promote written communication using modalities which may be less sensitive to disruption in these brain circuits, e.g. typing? Van Waelvelde et al. reported the unexpected finding that children who did not receive therapy improved in motor proficiency more than children who did receive therapy. While the authors reasonably consider the plausible possibility that children who received therapy had the poorest prognosis, this clearly highlights the urgent need for further research to elucidate the role and efficacy of interventions. Limited high quality evidence exists to guide clinicians in selecting interventions that address the motor difficulties of these children. Randomized controlled trials are needed to provide an empirical basis for the provision of motor interventions, including the content, optimal timing, and intensity.

The interesting findings of this study further highlight the need for well-designed prospective longitudinal studies over extended time periods, preferably from large population-based samples. Such studies would further clarify the population-based prevalence, extent, and developmental trajectory of motor impairment in those with ASD and ADHD. Together with genetic investigations, this approach will go some of the way to also addressing the vexing issue of comorbidity between children with ASD, ADHD, and developmental coordination disorder.

Ancillary