Date of Award

January 2019

Document Type

Open Access Thesis

Degree Name

Medical Doctor (MD)



First Advisor

Laura R. Ment


Survivors of preterm birth experience long-lasting behavioral problems characterized by increased risk of depression, anxiety, and impaired social functioning. The amygdala is a key region for social functioning, and alterations in amygdalar structure and connectivity are thought to underlie social functioning deficits in many disorders, including preterm birth. However, the trajectory of social impairments in PT and their association with functional connectivity of the amygdala are not well-studied in former preterm born individuals (PTs).

It was hypothesized that PTs would show impaired social functioning compared to term controls beginning in early childhood and continuing to young adulthood. It was also hypothesized that amygdala resting state functional connectivity is altered in PT born young adults, and that alterations in amygdala functional connectivity would mediate increased internalizing behavior and socialization problems in PT born young adults.

In a group of former very PT infants (600 to 1250 grams birth weight) and matched term (T) controls, measures of social and emotional behavior were examined using the Child Behavior Checklist (CBCL) administered at ages 8, 12, and 16, the Youth Self Report administered at age 16, and the Vineland Adaptive Behavior Scales (VABS) administered at ages 8 and 18. Amygdalar functional connectivity was examined using resting-state functional magnetic resonance imaging at age 20.

By parent report, preterm-born children and adolescents exhibit behaviors demonstrating increased social impairment compared to their term-born peers, starting at school-age and becoming more prominent by young adulthood. PT demonstrate a worsening trajectory in CBCL Withdrawn scores from school-age to young adulthood compared to T (group*time interaction p=0.03), and maternal education has a protective effect on this trajectory in the PT population (withdrawn group*time interaction p=0.01). Furthermore, amygdalar connectivity is altered in the formerly prematurely-born, and markers of social impairment correlate negatively with altered amygdala-posterior cingulate cortex connectivity (Social competence r=-0.37, p=0.03; socialization r=-0.42, p=0.01).

As this cohort of PTs does not include individuals who suffered any form of neurologic injury, their parent-reported increase in behavioral markers of social impairment may be attributable to prematurity rather than to neurologic injury. Moreover, these data suggest that previously established social impairments in PT as compared to T worsen during the critical period of transition from school-age to adolescence and suggest a possible neural underpinning for these impairments experienced by prematurely-born individuals.


This is an Open Access Thesis.

Open Access

This Article is Open Access