Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with a behavioral phenotype characterized by persistent deficits in social communication and social interaction accompanied by restricted, repetitive patterns of behaviors, interests, or activities. Currently in the US, approximately 2.5% of children have a diagnosis of ASD. The etiology of ASD is complex, however the disorder does have a strong genetic basis. Specific genetic mutations can lead to neuroanatomical and neurophysiological changes during development resulting in a behavioral phenotype that falls along the ASD spectrum and may result in a diagnosis of ASD. The severity of ASD-specific behaviors falls on a continuum and co-occurring psychiatric disorders are common – adding to the complexity of the disorder. In addition to specific gene mutations implicated in the diagnosis of ASD, specific brain regions are also implicated in ASD that are different from those observed in other common neurodevelopmental disorders – such as Attention-Deficit Hyperactivity Disorder. Studying the neuroanatomical footprint of ASD is a relatively new area of research fueled by the desire to bridge the gap between brain structure and function. Several brain regions implicated in the core social/communication deficits and repetitive behaviors associated with ASD are also involved in various aspects of motor control. These brain areas include cortical regions such as the primary motor cortex (M1), primary somatosensory cortex (S1), inferior parietal lobule (IPL), and subcortical structures that include the cerebellum and basal ganglia. These neuroanatomical findings are bolstered by several studies detailing a wide range of motor deficits in children and adults with ASD. Therefore, studying motor control may provide another means to study the neurological underpinnings of ASD. However, the meaningfulness of nearly all studies detailing motor control deficits in children with ASD is limited due to comparisons limited to a single typically developing (TD) control group. Therefore, the specificity of motor deficits in children with ASD is not well understood since intellectual and behavioral deficits – not specific to children with ASD – may also contribute to the observed motor deficits between children with ASD and TD controls. To overcome this limitation, the current dissertation project employs a cross-syndrome design that includes two additional clinical control groups of children with Fetal Alcohol Spectrum Disorder (FASD) and Attention-Deficit Hyperactivity Disorder (ADHD) with similar intellectual and behavioral impairments as children with ASD. Utilizing this novel approach, motor deficits specific to children with ASD may be identified, allowing for the generation of new hypotheses about the neurological underpinnings of ASD.

To bridge the gap between neuroscience and motor control in the study of ASD it is important to understand what findings from both fields of research reveal about ASD. Therefore, an extensive literature review (Chapter 1) is warranted to orient the reader to what is currently known about the underlying neurology and motor deficits associated with ASD. To detail the progression of knowledge about the neuroanatomical deficits associated with ASD, the literature review will funnel from general to more specific findings from animal-models of ASD and human patient studies. Following the neuroanatomical review, a detailed overview of findings from motor control studies on individuals with ASD will be reviewed and discussed in relation to the key neuroanatomical findings in children with ASD.

The overall purpose of this dissertation was to identify motor features specifically impaired in children with ASD using a cross-syndrome design. This dissertation explores the three different motor tasks that previous studies have shown to be impaired in children with ASD compared to TD controls. To examine the specificity of previously observed deficits, motor features were extracted from:​ (1) a precision-grip force tracking task;​ (2) a postural maintenance task;​ and (3) a manual dexterity task and compared between children with ASD and children with FASD, ADHD, and TD controls. The first study (Chapter 2) examines group differences in isometric precision-grip static force output features in children with ASD, FASD, ADHD, and TD controls. In this study, grip-force output was maintained at 15% of maximal voluntary contraction (MVC) and no group differences were observed for:​ (1) relative force accuracy;​ (2) relative variability;​ (3) complexity;​ or (4) frequency structure of the force signal. However, the relative proportion of low frequency oscillations (0-1 Hz) was significantly associated with force accuracy, variability, and complexity in the ASD-group only. In the second study (Chapter 3), dynamic force control features were examined using a ramp-up (0-25% MVC) and ramp-down (25-0% MVC) task. Compared to the TD group, the children with ASD demonstrated significantly:​ (1) greater relative error during ramp-up and ramp-down;​ (2) lower ramp-up force- complexity;​ and (3) greater relative error during transition between ramp-up and ramp-down phases. In the third study (Chapter 4), postural sway features during quiet stance and unipedal stance time were examined. Compared to the FASD, ADHD, and TD groups, the children with ASD demonstrated significantly:​ (1) greater postural sway area and (2) mediolateral (ML) sway magnitude. Furthermore, children with ASD group demonstrated significantly greater anteroposterior (AP) sway velocity between the TD and FASD groups, and lower ML sway complexity compared to the FASD group only. For unipedal stance, TD children had greater stance times compared to all clinical groups. However, postural sway area was associated with unipedal stance times only in the ASD group. In the fourth study (Chapter 5), manual dexterity of the dominant and non-dominant was examined. Children in the ASD group showed significantly:​ (1) worse dominant hand dexterity compared to TD controls and (2) worse non-dominant hand dexterity compared to children in the FASD and TD groups. Finally, hand performance asymmetry was significantly lower children with FASD than children without FASD.

In summary, this dissertation uses a cross-syndrome approach to identify motor features specifically impaired in children with ASD. Throughout the dissertation, several ASD-specific motor features were identified that align with current knowledge of neuroanatomical deficits associated with ASD. Furthermore, identification of ASD-specific motor features using biomechanics techniques may provide a means to quantitatively study the effects of various pharmacological, behavioral, and non-invasive brain stimulation interventions in clinical settings. Therefore, studying the motor system in children with ASD may have clinical importance due to challenges in quantifying changes in behaviors associated with ASD. In this dissertation, several ASD-specific motor features are identified that can be measured quickly in clinical settings. Further research is required to examine the clinical utility of quantitative motor testing in children with ASD.