The hypothesised primacy of motor development in developmental trajectories considered in the context of Autism Spectrum Disorders

Schafer et al propose that motor stereotypy (found in Autism Spectrum Disorder ASD) is a downstream manifestation of low motor complexity.9 The reduced exploratory motor drive evident in many ASD children, for example, is hypothesized to begin with these deficits in primary and secondary variability of movement, which cascade to motor coordination difficulties and impaired complex motor sequencing.10

Relative impoverishment of multisensory experiences in the first 100 days may trigger trajectories of sensory processing compensations. Synchronous multisensory experiences, including proprioceptive, haptic, visual, and auditory, enhance neural connectivity and sensory-motor processing.20 This paper hypothesizes that impoverishment of environmental stimulation, both social and non-social, chronic SNS-HPA hyperarousal, and disrupted parent-infant biobehavioral synchrony, result in trajectories of compensatory sensory hyper- or hypo-sensitivity and sensory seeking behaviors.

Applying the example of Autism Spectrum Disorder (ASD), up to 60% of children with ASD have motor deficits, including impaired postural control, impaired motor planning and sequencing, which affects gesture planning and imitation, and low motor tone.2, 3

Prospective or feedforward mechanisms of motor timing, also referred to as sensory-motor intentionality, are typically disrupted in ASD, as is perceptual awareness of others’ intentions conveyed in body movement or eye gaze. Torres et al argue that motor disruption is a core feature of ASD, requiring assessment methods suitable for inclusion in clinical diagnostic criteria.4

The NDC neurobiological model of infant development builds on the hypotheses concerning the primacy of either in-utero, intra-partum, or very early life motor lesions in ASD etiology, as detailed in ground-breaking syntheses by Delafield-Butt and Trevarthen, Dadalko and Travers, and Torres et al.5 These researchers propose that a structural (genetic or injury) or functional (monoaminergic) motor lesion is sustained in the brainstem systems or cortical subplate in the critically neuroplastic window in-utero, intra-partum, or in very early life, which impairs prospective, affect-driven movement. Cascades of imbalance between local and global connectivity emerge, resulting in atypical neurological, psychological, and behavioural development. Chronic SNS-HPS hyperarousal and disrupted parent-infant biobehavioral synchrony are key physiological and behavioural mechanisms which either predispose to very early motor lesions, or perpetuate the effects of very early motor lesions.

Studies corroborate the hypothesis that very early life motor lesions of the brainstem or cortical suplate initiate the atypical developmental trajectories of Autism Spectrum Disorder

A retrospective 2008 study of videos of 20 children diagnosed with ASD demonstrated impaired complexity and variability of general movements and absent or abnormal fidgety movements in infancy.1 A 2013 prospective, longitudinal study of 235 low and high-risk infants aged 6-36 months demonstrated developmental differences from 6 months of age, and poorer fine motor skills were evident in the high-risk infants by 14 months of age.2 3 In a 2014 study of 158 high-risk siblings and low risk infants, repetitive and stereotyped motor behaviour was observed as early as 12 months of age in high-risk siblings who are were diagnosed with ASD at 24 months of age.4 A 2017 comparative study of 71 low and high-risk infants showed that high-risk siblings who later develop learning delays have less variety of general movements in the first eight weeks post-birth, and less variety of movements in response to language, suggesting less flexible sensory-motor systems.5 A 2018 study comparing 86 high-risk siblings with 113 low risk infants showed that high-risk siblings who walked independently at 12 months of age had superior social-communication skills relative to high-risk siblings who weren’t walking. A 2019 prospective study of 437 high-risk siblings and 188 low risk infants were assessed at 6 months and 36 months. High-risk siblings have poorer fine motor skills and delayed motor development at 6 months, though these findings are not predictive of later diagnosis of ASD.6

References

1. Phagava H, Muratori F, Einspieler C, Maestro S, Apicella F, Guzzetta A, et al. General movements in infants with autism spectrum disorders. Georgian Medical News. 2008;156:100-105.
2. Landa RJ, Stuart EA, Gross AL, Faherty A. Developmental trajectories in children with and without Autism Spectrum Disorders: the first 3 years. Child Development. 2013;84(2):429-442.
3. Bradshaw J, Klaiman C, Gillespie S, Brane N, Lewis M, Saulnier C. Walking ability is associated with social communication skills in infants at high risk for Autism Spectrum Disorder. Infancy. 2018;23(5):674-691.
4. Elison JT, Wolff JJ, Reznick JS, Botteron KN, Estes AM, Gu H, et al. Repetitive behavior in 12-month-olds later classified with Autism Spectrum Disorder. Journal of American Academy of Child and Adolescent Psychiatry. 2014;53(11):1216-1224.
5. Denisova K, Zhao G. Inflexible neurobiological signatures precede atypical development in infants at high risk for autism. Scientific Reports. 2017;7(1):11285.
6. Iverson JM, Shic F, Wall CA, Chawarska K, Curtin S, Estes A, et al. Early motor abilities in infants at heightened versus low risk for ASD: a baby siblings research consortium (BSRC) study. Journal of Abnormal Child Psychology. 2019;128(1):69-80.

Delafield-Butt JT, Trevarthan C. On the brainstem origin of autism: disruption to movements of the primary self. In: Torres EB, Whyatt C, editors. Autism: the movement sensing perspective: Taylor and Francis CRC Press; 2017.

Other references for this excerpt are found in:

Douglas PS. Pre-emptive intervention for autism spectrum disorder: theoretical foundations and clinical translation. Frontiers in integrative neuroscience. 2019;13: https://doi.org/10.3389/fnint.2019.00066.