Poster #5 - Role of the amygdala and hippocampus in the development of anxiety disorders in young children with and without sensory over-responsivity

• In Event: Poster Session 15

Abstract

Background: Sensory over-responsivity is an early predictor in young children for the development of anxiety disorders, particularly generalized anxiety disorder. Research in the fields of sensory over-responsivity and anxiety have both separately demonstrated a role for the limbic system, particularly the hippocampus and amygdala, in these conditions. However, to date no one has explored whether differences in the size of the amygdala and hippocampus are associated with the development of anxiety in children with and without sensory over-responsivity. Understanding this relationship could provide information about the underlying neurobiological mechanisms by which sensory over-responsivity leads to the development of anxiety disorders in young children.

Methods: Children’s sensory and anxiety symptoms were assessed in a community sample of 917 2-to-5-year old preschoolers and again in 191 of these children at 6 years old. Of these children, 94 (42 females/52 males) also received a T1-weighted MRI scan when they were between 5 and 10 years old (mean 6.9 years old). Volumes of the amygdala and hippocampus, corrected for total intracranial volume, were computed using FreeSurfer version 6.0. The relationship between sensory over-responsivity at preschool, brain volume at school-age, and school-age anxiety was tested through a series of general linear models and logistic regressions. Analyses controlled for age at brain scan, sex, and race.

Results: Sensory over-responsivity and anxiety were each independently associated with the size of the right amygdala and the bilateral hippocampus. Specifically, a smaller right amygdala was associated with higher levels of anxiety symptoms (β (SE) = -1110 (540), p < .05) and more symptoms of sensory over-responsivity (β (SE) = -2629 (1241), p < .05). Similarly, a smaller hippocampus was associated with higher levels of anxiety symptoms (β (SE) = -550 (153), p < .001) and more symptoms of sensory over-responsivity (β (SE) = -636 (225), p = .05). The hippocampus moderated the relationship between preschool sensory over-responsivity and later anxiety symptoms. Specifically, there was an interaction between hippocampal size and sensory over-responsivity (β (SE) = 321 (148), p < .05), with a smaller hippocampus associated with more anxiety symptoms in the children without sensory over-responsivity (β (SE) = -811 (214), p < .001). The same interaction was not seen for the amygdala.

Conclusion: Smaller amygdala and hippocampi are each independently associated with both sensory over-responsivity and anxiety. However, the size of the hippocampus is only associated with anxiety symptoms in children without sensory over-responsivity. This suggests that, while the hippocampus and amygdala are implicated in both sensory over-responsivity and anxiety, the pathway between sensory over-responsivity and anxiety is not significantly related to hippocampal and amygdala size.

Authors

• Kimberly Carpenter, Duke Univeristy
  Presenting Author

• William Copeland, University of Vermont

• Adjoa T Ewool, Duke Univeristy

• Kathryn Garrisi, University of North Carolina at Chapel Hill

• Connor Haughey

• Luong Huynh

• Sarah Maren Lempres, Duke Univeristy

• Esmeralda Navarro, University of North Carolina Chapel Hill

• Helen Egger, New York University Langone, Child Study Center

• Margaret A. Sheridan, University of North Carolina at Chapel Hill