Search
Program Calendar
Browse By Day
Browse By Time
Browse By Panel
Browse By Session Type
Browse By Topic Area
Search Tips
Virtual Exhibit Hall
Personal Schedule
Sign In
X (Twitter)
A substantial body of research has delineated links between chronic stress exposure and childhood deficits in cognitive function (Pechtel, 2011). This work has been important for highlighting the relevance of the early environment to cognitive development and identifying repetitive/chronic stress as a pathway through which experience imprints on cognition (McEwen, 2013). Missing, however, is an examination of the impact of temporally-proximal acute stressors on children’s cognitive function, which may be relevant for understanding long-term deficits observed in individuals with repetitive stress exposure.
Theory suggests that acute stress biases cognitive function towards more indiscriminately reactive states, with adult neuroimaging research highlighting alterations in early attentional processes, even after a stressor has ended (Sanger, 2014). We hypothesized that acute stress would impair children’s sustained attention performance. We did not have directional hypotheses about the presence of the effect of stress on inhibitory control (i.e., No-go performance), given mixed evidence for impairment in adults (Shields, 2016). Parenting stress was also hypothesized to be associated with children’s cognitive and autonomic nervous system vulnerability to acute stress, given the critical role of primary caregivers in supporting the development of children’s stress-regulatory capacity and cognitive function (Bridgett, 2015).
Here, the effects of acute stress on sustained attention and inhibitory control, as measured in a Go/No-go task, were examined in young children (M age = 5.41 years). Given the critical role of the parent-child relationship to children’s self-regulatory development, the extent to which parenting stress predicts children’s cognitive vulnerability to acute stress and autonomic reactivity (i.e., sympathetic nervous system, SNS and parasympathetic nervous system, PNS) was also investigated. A between-groups design (n=58 stress, n=26 control) was used with oversampling of the stressor-exposed children to examine individual differences. A validated socially-evaluative ‘matching task’ game was used as an acute stressor, with a non-evaluative matching task game for control. The Parenting Stress Index and subscales were employed as a measure of parenting stress.
As determined by a repeated measures ANOVA, acute stress impaired children’s sustained attention, but not inhibitory control (time × trial type × condition [F(1,72) = 4.17, p = .045], with planned simple effects indicating a decrease in Go trial performance for the stressor group [F(1,72) = 4.47, p =.038)] and no change for the control group (Figure 1). There were no changes in No-go performance for either group. Higher parenting stress was associated with attentional impairment [r(47) = -.34, p =.02; Figure 2]. Parenting distress was positively associated with SNS reactivity to acute stress (r = -.45, p =.004), but neither SNS nor PNS reactivity was associated with attentional impairment.
A conceptual model of pathways through which repetitive acute stress may contribute to self-regulatory difficulties is presented, including the potential buffering role of caregivers. Establishing the extent to and mechanisms by which acute stress alters children’s cognition may allow us to understand the contexts in which children are more likely to have difficulties and identify candidate processes, such as acute stress management, for targeted intervention research to support children’s function.
Leslie Elizabeth Roos, University of Manitoba
Presenting Author
Ryan Giuliano, University of Manitoba
Non-Presenting Author
Kate Beauchamp, University of New Mexico School of Medicine
Non-Presenting Author
Elliot Berkman, University of Oregon
Non-Presenting Author
Erik Knight, The Pennsylvania State University
Non-Presenting Author
Philip Fisher, University of Oregon
Non-Presenting Author