Thesis (B.A.Hons.))--University of Adelaide, Dept. of History, 1981. / Typescript (photocopy).

Thesis (M.S.)--University of Michigan, 1993.

Thesis (M.S.)--University of Michigan, 1993.

Doctoral dissertation. / Format: PDF. Bibl.

Thesis (M.P.H.)--University of Michigan, 1946.

Thesis (M.P.H.)--University of Michigan, 1946.

<p>  </p> <p>Dyadic play interactions are a cornerstone of early development and difficulty engaging in sustained synchronous interactions are linked to later difficulties with language and joint attention. For children at elevated risk for autism spectrum disorder (ASD), it is unclear if early difficulties in synchronous exchanges could inform later diagnoses. As part of a prospective monitoring study, infant siblings of children with ASD (high-risk group) or typical development (low-risk group), and their mothers completed a standardized play task. Play interactions for infants were evaluated to: (1) assess if early difficulties with social responsiveness or synchrony proceed ASD diagnoses within the first year; (2) explore whether repertoires of observed synchronous behaviors distinguish ASD-risk; and (3) examine whether the unfolding rates of synchrony and responsiveness over continuous time highlight ASD-risk differences. </p> <p><br></p> <p>By 12 months, distinct mean-level differences in synchrony and responsiveness by risk status were observed. Higher synchrony and responsiveness totals were also positively associated with infants later language and cognitive scores and negatively associated with ASD symptom severity (Chapter 2). Although, dyads utilized mostly comparable repertoires of observed synchronous and responsive behaviors, regardless of group membership (Chapter 3). And lastly, the overall rates of unfolding synchrony and responsiveness were fairly stable throughout the interaction. However, distinct patterns by ASD-risk and developmental outcomes were evident (Chapter 4). Ultimately, the encompassed studies did not consistently find robust ASD-specific differences. However, these studies did demonstrate the applicability of advanced methodologies to provide relevant contextual/dyadic elements (beyond the field’s norm of mean-level totals), particularly for infants with non-autism developmental concerns. Future research should build upon these studies to assess synchrony and responsiveness growth curves that extend beyond 12 months of age, as well as utilize behavioral coding approaches that systematically capture both synchronous and asynchronous exchanges.</p>

<p>The manifestations of early sleep disturbances on cerebrospinal fluid and their relations with early developmental competencies are understudied. Recent studies highlight cerebrospinal fluid disbursement as a potential factor associated with dysfunctions in brain development. With two studies, we explored sleep and extra-axial cerebrospinal fluid (EA-CSF) connection as a potential mechanistic pathway by which sleep dysregulation influences brain and behavior development. Specifically, we evaluated associations between (1) EA-CSF to total cerebral volume (EA-CSF/TCV) ratios, (2) parent-report of child sleep problems, and (3) social communication development in typical (Study 1) and atypical populations (Study 2). In typical infants, early sleep problems did not precede later elevated EA-CSF/TCV ratios or social-communicative competence. Elevated EA-CSF/TCV ratios were associated with impaired social communication skills, suggesting that a relationship between elevated EA-CSF/TCV ratios and social communication impairments exists regardless of neurological or sleep problems. In an atypical population with autism spectrum disorder (ASD), older children with ASD had similar EA-CSF/TCV ratios to a group of their typically developing peers. Sleep problems were negatively associated with EA-CSF/TCV ratios but positively associated with social-communicative impairments for children with ASD, highlighting the influence of sleep problems on both brain and behavioral outcomes in an atypical population. In both studies, EA-CSF volumes continue to increase during early development in the typically developing populations (but not later in the atypical sample), underlining its relevance as a marker of atypical processing. Recognizing the potential roles of EA-CSF in influencing several biosocial and behavioral aspects of development, we encourage researchers to continue to explore EA-CSF growth, especially during developmental periods of flux and transition. Future work with longitudinal data can also serve to explore sleep-related developmental changes in EA-CSF, in association with behavioral and phenotypic changes. </p>