Disruptions in stress response system development have been posited as mechanisms linking child maltreatment (CM) to psychopathology. Existing theories predict elevated sympathetic nervous system reactivity after CM, but evidence for this is inconsistent. We present a novel framework for conceptualizing stress reactivity after CM that uses the biopsychosocial model of challenge and threat. We predicted that in the context of a social-evaluative stressor, maltreated adolescents would exhibit a threat pattern of reactivity, involving sympathetic nervous system activation paired with elevated vascular resistance and blunted cardiac output (CO) reactivity.
A sample of 168 adolescents (mean age =14.9 years) participated. Recruitment targeted maltreated adolescents; 38.2% were maltreated. Electrocardiogram, impedance cardiography, and blood pressure were acquired at rest and during an evaluated social stressor (Trier Social Stress Test). Pre-ejection period (PEP), CO, and total peripheral resistance reactivity were computed during task preparation, speech delivery, and verbal mental arithmetic. Internalizing and externalizing symptoms were assessed.
Maltreatment was unrelated to PEP reactivity during preparation or speech, but maltreated adolescents had reduced PEP reactivity during math. Maltreatment exposure (F(1,145) = 3.8–9.4, p = .053–<.001) and severity (β = −0.10–0.12, p = .030–.007) were associated with significantly reduced CO reactivity during all components of the stress task and marginally associated with elevated total peripheral resistance reactivity (F(1,145) = 3.8–9.4; p = .053–<.001 [β = 0.07–0.11] and p = .11–.009, respectively). Threat reactivity was positively associated with externalizing symptoms.
CM is associated with a dysregulated pattern of physiological reactivity consistent with theoretical conceptualizations of threat but not previously examined in relation to maltreatment, suggesting a more nuanced pattern of stress reactivity than predicted by current theoretical models.
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From the Department of Psychology (K.A.M.), University of Washington, Seattle, Washington; Developmental Medicine Center (M.A.S.), Boston Children’s Hospital, Boston, Massachusetts; Department of Pediatrics (M.A.S.), Harvard Medical School, Boston, Massachusetts; Harvard Graduate School of Education (S.A.), Cambridge, Massachusetts; and Department of Psychiatry (W.B.M.), University of California San Francisco, San Francisco, California.
Address correspondence and reprint requests to Katie A. McLaughlin, PhD, Department of Psychology, University of Washington, Box 351525, Seattle, WA 98195. E-mail: firstname.lastname@example.org
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Received for publication September 26, 2013; revision received June 14, 2014.