Background and objectives: After a previous report demonstrated blunted heart rate (HR) reactivity in association with adverse childhood experiences (ACEs) [Voellmin, A., Winzeler, K., Hug, E., Wilhelm, F. H., Schaefer, V., Gaab, J., … Bader, K. (2015). Blunted endocrine and cardiovascular reactivity in young healthy women reporting a history of childhood adversity. Psychoneuroendocrinology, 51, 58–67. doi:10.1016/j.psyneuen.2014.09.008], the present analysis aimed at clarifying the role of the sympathetic and parasympathetic branches of the autonomic nervous system in this relationship. Design and Methods: One hundred eighteen healthy young women provided data on ACEs and underwent psychosocial stress testing. Systolic blood pressure (SBP) and respiratory sinus arrhythmia (RSA, quantified by high-frequency HR variability) were assessed as measures of sympathetic and parasympathetic cardiovascular activity, respectively. A mediation model was calculated to test the indirect effects of ACEs on HR via SBP and RSA. Results: The effect of ACEs on HR reactivity was mediated by SBP reactivity but not by RSA reactivity. ACEs were associated with reduced SBP at rest. Conclusions: ACEs were associated with down-regulation in a measure of sympathetic but no alteration in a measure of parasympathetic cardiovascular stress reactivity in adulthood. Future research will need to clarify whether this indicates risk or resilience.

The present study examined to what extent adverse childhood experiences (ACE), in addition to demographic characteristics, current level of stress, depression, and arousability predisposition, are associated with sleep measures in adult insomnia. Thirty-nine adults suffering from primary insomnia completed self-report questionnaires assessing ACE, current level of stress, predisposition towards increased arousability, and depression. They were monitored for 7 consecutive nights at home with wrist actigraphs to evaluate objective sleep-related activity. Blockwise multiple regression analyses were performed to determine which variables were the most important predictors of sleep measures. ACE proved to be important predictors of actigraphically assessed sleep onset latency, sleep efficiency, number of body movements, and moving time, whereas the set of the remaining variables had no significant impact on these sleep measures. These findings suggest that there is an association between childhood maltreatment history and sleep in patients with primary insomnia. We presume that sleep-related nightly activity can be regarded as an aftereffect of long-lasting stressful experiences in childhood.

Summary: The present study explores the relationship between childhood maltreatment experiences and spectral power in high-frequency EEG activity during sleep in a sample of adults experiencing primary insomnia. Forty-five nontreated patients with primary insomnia spent three consecutive nights in the sleep laboratory, during which polysomnographic recordings were carried out. Nonrapid eye movement and rapid eye movement EEG data were analyzed using spectral analysis. In addition, each participant completed several self-report questionnaires assessing maltreatment in childhood and adolescence, current level of stress, and current depressivity. Insomnia patients with self-reported history of moderate to severe childhood maltreatment (MAL group; n = 25), as measured by the Childhood Trauma Questionnaire, were compared with insomnia patients without such a history (non-MAL group; n = 20). The MAL group exhibited more absolute and relative beta 1 and beta 2 power in nonrapid eye movement sleep and more absolute beta 1 and beta 2 activity in rapid eye movement sleep than the non-MAL group. Contrary to hypothesis, no group differences were found in gamma frequency band. The results suggest an association between history of childhood maltreatment and increased beta EEG activity particularly during nonrapid eye movement sleep in adult insomnia, what may reflect heightened psychophysiologic arousal during sleep.