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- Creators: Department of Psychology
- Creators: Ortiz, J. Bryce
Description
Children's chronic pain has many contributing factors, including family environment, genetics, and parenting. Still, pediatric chronic pain remains understudied, and little research has been conducted on predictors of child pain onset. This study aims to elucidate some of these factors by examining the role of parenting style and parental pain in children's chronic pain experience. The study answered the following questions: 1) Is child chronic pain heritable?; 2) Do parenting styles and/or parental pain predict child pain?; and 3) Is parenting style the mediating variable in the relation between parent pain and child pain? A twin study design was employed to account for both genetic and environmental influences in pain. Primary and secondary caregivers completed pain questionnaires regarding their own and their children's pain. The caregivers also completed questionnaires regarding their own parenting styles. Observer ratings were used as additional measures of primary caregiver parenting. Results indicated that child pain is heritable and that parental pain was significantly related to child pain. However, parenting style did not predict child pain and was not a mediator in the relationship between parental pain and child pain. Further research on other parenting factors or predictors of pain may lead to prevention of pediatric chronic pain or more effective management of child pain symptoms.
ContributorsPatel, Maya (Author) / Davis, Mary (Thesis director) / Lemery, Kathryn (Thesis director) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Neuroinflammation Following Experimental Diffuse Brain Injury in Pre-pubertal and Peri-pubertal Rats
Description
Traumatic brain injury is the leading cause of mortality and morbidity in children and adolescents. Adolescence is a critical time in development where the body and brain undergoes puberty, which not only includes reproductive maturation, but also adult social and cognitive development. Brain-injury-induced disruptions can cause secondary inflammation processes and as a result, pediatric TBI can lead to significant life-long and debilitating morbidities that continue long after initial injury. In this study, neuroinflammation following diffuse brain injury was explored in prepubertal and peripubertal rats using an adapted method of midline fluid percussion injury (mFPI) for juvenile rats to further understand the relationship between pediatric TBI and puberty disruption due to endocrine dysfunction. We expect the adapted mFPI model to be effective in producing diffuse, moderate brain injury in juvenile rats and hypothesize that pre-pubertal rats (PND35) will have increased neuroinflammation compared to peri-pubertal rats (PND17) and shams because of the potential neuroprotective nature of sex steroids. Male Sprague-Dawley rats (n=90) were subjected to either a diffuse midline fluid percussion injury (mFPI) or sham injury at post-natal day (PND) 17 (pre-puberty) or PND35 (peri-puberty). Animals were sacrificed at different time points defined as days post injury (DPI) including 1DPI, 7DPI and 25DPI to represent both acute and chronic time points, allowing for comparisons within groups (injury vs. sham) and across groups (PND17 vs PND35). Body weight of the rats was measured postoperatively at various time points throughout the study to follow recovery. Tissue was collected and subjected to Heamatoxylin and Eosin (H&E) stain to visualize histology and evaluate the application of diffuse mFPI to juvenile rats. In addition, tissue underwent immunohistochemical analysis using 3,3'-diaminobenzidine (DAB) to stain for ionized calcium binding proteins (Iba1) in order to assess injury-related neuroinflammation in the form of microglia activation. Diffuse brain injury using the mFPI model did not affect rat body weight or cause overt cell death, suggesting adaption of the adult mFPI model for juvenile rats is representative of moderate diffuse brain injury. In addition, diffuse TBI lead to morphological changes in microglia suggesting there is an increased inflammatory response following initial insult, which may directly contribute to improper activation of pubertal timing and progression in adolescent children affected. Since there is little literature on the full effects of puberty dysfunction following TBI in the pediatric population, there is a significant need to further assess this area in order to develop improved interventions and potential therapies for this affected population.
ContributorsNewbold, Kelsey Bevier (Author) / Newbern, Jason (Thesis director) / Rowe, Rachel (Committee member) / Ortiz, J. Bryce (Committee member) / School of Mathematical and Natural Sciences (Contributor) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
Chronic stress often leads to cognitive deficits, especially within the spatial memory domain mediated by the hippocampus. When chronic stress ends and a no-stress period ensues (i.e., washout, WO), spatial ability improves, which can be better than non-stressed controls (CON). The WO period is often the same duration as the chronic stress paradigm. Given the potential benefit of a post-stress WO period on cognition, it is important to investigate whether this potential benefit of a post-stress WO period has long-lasting effects. In this project, chronic restraint (6hr/d/21d) in Sprague-Dawley rats was used, as it is the minimum duration necessary to observe spatial memory deficits. Two durations of post-stress WO were used following the end of chronic restraint, 3 weeks (STR-WO3) and 6 weeks (STR-WO6). Immediately after chronic stress (STR-IMM) or the WO periods, rats were tested on various cognitive tests. We corroborated past studies that chronic stress impaired spatial memory (STR-IMM vs CON). Interestingly, STR-WO3 and STR-WO6 failed to demonstrate improved spatial memory on a radial arm water maze task, performing similarly as STR-IMM. Performance outcomes were unlikely from differences in anxiety or motivation because rats from all conditions performed similarly on an open field task and on a simple object recognition paradigm, respectively. However, performance on object placement was unusual in that very few rats explored, suggesting some degree of anxiety or fear in all groups. One possible interpretation of the unusual results of the 3 week washout group may be attributed to the different spatial memory tasks used across studies or external factors from the study. Further exploration of these other factors led to the conclusion that they did not play a role and the STR-WO3 RAWM data were anomalous to other studies. This suggests that a washout period following chronic stress may not be fully understood.
ContributorsFlegenheimer, Aaron Embden (Author) / Conrad, Cheryl (Thesis director) / Bimonte-Nelson, Heather (Committee member) / Ortiz, J. Bryce (Committee member) / School of Life Sciences (Contributor) / School of Human Evolution and Social Change (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
Description
Early childhood environment is critical to subsequent physical health in children and is influenced by children's primary caregivers \u2014 typically mothers. Maternal stress, one aspect of a child's environment, may shape the functioning of the child's physiological stress response system, which has been linked to later health outcomes, including pain. The current study evaluated whether: 1) early maternal stress, defined as maternal depressive symptoms and low socio-economic status, predicts later child pain; 2) early maternal stress relates to later child daily cortisol output; and 3) child's cortisol output across the day mediates the relation between early maternal stress and child pain. Maternal stress was assessed via questionnaires at twin age 12-months. At twin age seven years, twins' salivary cortisol was collected three times per day for three days. At twin age nine years, twins rated how often they experienced stomach, headache, and back pain weekly or more frequently. Results of multilevel linear and logistic regression analyses showed that early maternal stress did not predict later children's daily cortisol output or extent of child pain. Therefore, findings were inconsistent with the proposed mediation model. However, there was a marginally significant negative relation between child daily cortisol output and later extent of child pain. Current findings suggest that functioning of the stress response system, reflected in cortisol output, may have implications for the development of child pain. Future work evaluating intensely stressful early environments may provide clues about the links between a child's early environment and the development of his/her stress response system.
ContributorsRoth, Winter Rayne Nicole (Author) / Davis, Mary (Thesis director) / Miadich, Samantha (Committee member) / Department of Psychology (Contributor) / School of Molecular Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-12