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Poster #40 - Autonomic Regulation in a High-Risk Sample of Young Adolescents during a Social Stress Task

Thu, April 12, 10:15 to 11:15am, Hilton, Floor: Second Floor, Marquette Ballroom

Abstract/Description

Prenatal exposure to cocaine (PCE) has been increasingly linked to deficits in the development of regulatory processes from infancy into childhood but less is known about regulation during adolescence when neural rewiring may either exacerbate or ameliorate the earlier effects of PCE. The regulatory system is complex and may be reflected in autonomic (ANS) systems. The sympathetic branch (SNS) of the ANS can be measured via pre-ejection period (PEP) while the parasympathetic branch (PNS) is commonly measured by respiratory sinus arrhythmia (RSA; Bernstein et al., 1997; Porges, 1995). For both PEP and RSA, baseline measures and measures of change in response to environmental challenge have been used to assess psychological regulation. The purpose of this study was to examine the association between PCE and PEP/RSA during the Trier Social Stress Task (TSST: Kirschbaum, Pirke, & Hellhammer,1993), a laboratory paradigm designed to elicit social stress in young adolescents (M = 13.87 years, SD = .34; 57% female).
Participants consisted of 66 adolescents (34 cocaine-exposed, 32 nonexposed) participating in an ongoing longitudinal study of prenatal cocaine exposure. See Table 1 for sample characteristics. Prenatal substance exposure was ascertained by a combination of self-report, maternal hair, and urine toxicology assessments at delivery. The TSST consisted of 4 epochs: a 5-minute baseline (watching a relaxation video), 4-minute anticipation (preparing a speech using a prompt), 4-minute speech and 4-minute serial subtraction task performed in front of judges. RSA and PEP were collected continuously during each epoch and analyzed using Impedance and Heart Rate Variability software from Mindware Technologies (Gahann, OH). Adolescents also self-reported their stress levels using a 5-point rating scale after the relaxation video and after the speech and math portions of the TSST.
A repeated-measures ANCOVA with prenatal exposure status as the independent variable and other prenatal exposure as covariates indicated a significant epoch by group status effect, F(3,61) = 2.896, p = .047, η2p = .08 (see Figure 1) for RSA. Simple effects analyses indicated that RSA was not different between groups for baseline and the anticipation epoch but the exposed group had a significantly larger decrease in RSA during the speech epoch and remained marginally lower than the nonexposed group during the math epoch. Repeated-measures ANCOVAs for PEP and the stress ratings yielded no significant effects.
The failure to find group differences in PEP suggests that prenatal cocaine exposure may not be directly related to differences in sympathetic activation during social stress. One possible explanation is that the TSST was not stressful enough to activate the sympathetic nervous system, an interpretation that is supported by the fact that there were no significant increases in reported stress levels over time. Although we did not find any group differences in RSA during baseline or speech preparation, we did find that adolescents who were prenatally exposed to cocaine had increased RSA reactivity (greater suppression) during the TSST speech, indicating greater parasympathetic nervous system activation. Results highlight the importance of examining individual components of the regulatory system.

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