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Cortical asymmetry as a potential link between depressive symptoms and cardiovascular reactivity
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Betensky, Julia. Cortical asymmetry as a potential link between depressive symptoms and cardiovascular reactivity. Retrieved from https://doi.org/doi:10.7282/T3T1540F

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TitleCortical asymmetry as a potential link between depressive symptoms and cardiovascular reactivity
NameBetensky, Julia (author); Contrada, Richard J. (chair); Wilson, Terence (internal member); Kusnecov, Alexander (internal member); Rutgers University; Graduate School - New Brunswick
Date Created2008
Other Date2008-10 (degree)
SubjectPsychology, Psychophysiology, Depression, Mental, Cardiovascular system--Diseases--Psychosomatic aspects
Extentvii, 37 pages
DescriptionAlthough depression appears to be an independent risk factor for cardiovascular morbidity and mortality, the mechanisms by which emotion dysregulation leads to cardiovascular disease (CVD) are largely unclear. One suggestion that has received considerable attention is that depression promotes cardiovascular reactivity, which is hypothesized to contribute to CVD over time (Blascovich & Katkin, 1993; Krantz & Manuck, 1984). There are putative neurobiological pathways by which the brain communicates with the heart during the processing of emotion and stress. Prefrontal cortical asymmetry appears to be an objective physiological index of a depressive affective style that may promote autonomic nervous system dysregulation. In the proposed study, cortical asymmetry was examined as a predictor of cardiovascular reactivity. Sixty-four healthy female undergraduate students completed the Beck Depression Inventory-II (Beck et al., 1996) and a speech stressor task, in which they were asked to recall a personally-relevant event that made them feel depressed. It was hypothesized that greater self-reported depression would be associated with right-lateralized prefrontal cortical asymmetry, and that this asymmetry would be associated with increased systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) at rest and during the speech. Results indicated that greater self-reported depression was neither associated with right-dominant prefrontal cortical asymmetry nor cardiovascular resting activity nor reactivity to the stressor. Although several analyses also revealed that cortical asymmetry did not moderate the effect of depression on cardiovascular reactivity, right dominant midfrontal cortical activity was a significant predictor of increased DBP reactivity to the speech stressor when electrocortical activity was treated as a categorical variable. Continued investigation of cortical asymmetry as a potential link between clinical depression and increased vascular resistance may be useful in clarifying the utility of EEG measures of depression and for identifying high-risk groups for CVD.
NoteM.S.
NoteIncludes bibliographical references (p. 30-35).
Genretheses, ETD graduate
Persistent URLhttps://doi.org/doi:10.7282/T3T1540F
LanguageEnglish
CollectionGraduate School - New Brunswick Electronic Theses and Dissertations
Organization NameNjNbRU
RightsThe author owns the copyright to this work.
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