Abstract

No two individuals with the autism diagnosis are ever the same – yet many practitioners and parents can recognize signs of ASD very rapidly with the naked eye. What, then, is this phenotype of autism that shows itself across such distinct clinical presentations and heterogeneous developments? The “signs” seem notoriously slippery and resistant to the behavioral threshold categories that make up current assessment tools. Part of the problem is that cognitive and behavioral “abilities” typically are theorized as high-level disembodied and modular functions – that are assessed discretely (impaired, normal, enhanced) to define a spectral syndrome. Even as biology reminds us that organic developing bodies are not made up of independent switches, we remain often seduced by the simplicity of mechanistic and cognitive models. Developmental disorders such as autism have accordingly been theorized as due to different modular dysfunctions -typically of cortical origin, i.e. failures of “theory of mind” (Baron-Cohen et al., 1985), of the “mirror neuron system” (Ramachandran and Oberman, 2006), of “weak central coherence”(Happe and Frith, 2006) or of the balance of “empathizing” and “systemizing” (Baron Cohen, 2009), just to list a few. The broad array of autonomic (Ming et al., 2005;Cheshire, 2012) and sensorimotor (Damasio and Maurer, 1978;Maurer and Damasio, 1982;Donnellan and Leary, 1995;Leary and Hill, 1996;Donnellan et al., 2012) differences experienced and reported by people with autism have by such theories typically been sidelined as “co-morbidities”, possibly sharing genetic causes, but rendered as incidental and decisively behaviorally irrelevant symptoms –surely disconnected from cognition. But what if the development of cortically based mental processes and autonomous control relies on the complexities and proper function of the peripheral nervous systems? Through such an “embodied” lense the heterogeneous symptoms of autism invites new interpretations. We propose here that many behavioral-level findings can be re-defined as downstream effects of how developing nervous systems attempt to cope and adapt to the challenges of having various noisy, unpredictable and unreliable peripheral inputs.

Highlights

  • THE DISEMBODIED-STATIC BRAIN APPROACH TO ASD No two individuals with the autism diagnosis are ever the same—yet many practitioners and parents can recognize signs of ASD very rapidly with the naked eye

  • What if the development of cortically based mental processes and autonomous control relies on the complexities and proper function of the peripheral nervous systems? Through such an “embodied” lens the heterogeneous symptoms of autism invites new interpretations

  • We propose here that many behavioral-level findings can be re-defined as downstream effects of how developing nervous systems attempt to cope and adapt to the challenges of having various noisy, unpredictable, and unreliable peripheral inputs

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Summary

Introduction

THE DISEMBODIED-STATIC BRAIN APPROACH TO ASD No two individuals with the autism diagnosis are ever the same—yet many practitioners and parents can recognize signs of ASD very rapidly with the naked eye. We propose here that many behavioral-level findings can be re-defined as downstream effects of how developing nervous systems attempt to cope and adapt to the challenges of having various noisy, unpredictable, and unreliable peripheral inputs. Such experiences of living and coping with ASD, along with the widespread reports of sensorimotor and autonomic differences have led us to explore the hypothesis that individuals with autism are coping with unreliable peripheral signals from atypically self-organized subsystems.

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