Matching Items (4)
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- All Subjects: PTSD
- Creators: Chassin, Laurie
- Creators: Allen, Kelly Anne
- Creators: Bimonte-Nelson, Heather A.
- Member of: Theses and Dissertations
Description
An increasing number of military veterans are enrolling in college, primarily due to the Post-9/11 GI Bill, which provides educational benefits to veterans who served on active duty since September 11, 2001. With rigorous training, active combat situations, and exposure to unexpected situations, the veteran population is at a higher risk for traumatic brain injury (TBI), Post Traumatic Stress Disorder (PTSD), and depression. All of these conditions are associated with cognitive consequences, including attention deficits, working memory problems, and episodic memory impairments. Some conditions, particularly mild TBI, are not diagnosed or treated until long after the injury when the person realizes they have cognitive difficulties. Even mild cognitive problems can hinder learning in an academic setting, but there is little data on the frequency and severity of cognitive deficits in veteran college students. The current study examines self-reported cognitive symptoms in veteran students compared to civilian students and how those symptoms relate to service-related conditions. A better understanding of the pattern of self-reported symptoms will help researchers and clinicians determine the veterans who are at higher risk for cognitive and academic difficulties.
ContributorsAllen, Kelly Anne (Author) / Azuma, Tamiko (Thesis director) / Gallagher, Karen (Committee member) / Department of Speech and Hearing Science (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05
Description
The present study utilized longitudinal data from a high-risk community sample (n= 377; 166 trauma-exposed; 54% males; 52% children of alcoholics; 73% non-Hispanic/Latino Caucasian; 22% Hispanic/Latino; 5% other ethnicity) to test a series of hypotheses that may help explain the risk pathways that link traumatic stress, posttraumatic stress disorder (PTSD) symptomatology, and problematic alcohol and drug use. Specifically, this study examined whether pre-trauma substance use problems increase risk for trauma exposure (the high-risk hypothesis) or PTSD symptoms (the susceptibility hypothesis), whether PTSD symptoms increase risk for later alcohol/drug problems (the self-medication hypothesis), and whether the association between PTSD symptoms and alcohol/drug problems is due to shared risk factors (the shared vulnerability hypothesis). This study also examined the roles of gender and ethnicity in these pathways. A series of logistic and negative binomial regressions were performed in a path analysis framework. A composite pre-trauma family adversity variable was formed from measures of family conflict, family life stress, parental alcoholism, and other parent psychopathology. Results provided the strongest support for the self-medication hypothesis, such that PTSD symptoms predicted higher levels of later alcohol and drug problems among non-Hispanic/Latino Caucasian participants, over and above the influences of pre-trauma family adversity, pre-trauma substance use problems, trauma exposure, and demographic variables. Results partially supported the high-risk hypothesis, such that adolescent substance use problems had a marginally significant unique effect on risk for assaultive violence exposure but not on overall risk for trauma exposure. There was no support for the susceptibility hypothesis, as pre-trauma adolescent substance use problems did not significantly influence risk for PTSD diagnosis/symptoms over and above the influence of pre-trauma family adversity. Finally, there was little support for the shared vulnerability hypothesis. Neither trauma exposure nor preexisting family adversity accounted for the link between PTSD symptoms and later substance use problems. These results add to a growing body of literature in support of the self-medication hypothesis. Findings extend previous research by showing that PTSD symptoms may influence the development of alcohol and drug problems over and above the influence of trauma exposure itself, preexisting family risk factors, and baseline levels of substance use.
ContributorsHaller, Moira (Author) / Chassin, Laurie (Thesis advisor) / Davis, Mary (Committee member) / Pina, Armando (Committee member) / Tein, Jenn-Yun (Committee member) / Arizona State University (Publisher)
Created2014
Description
Contemporary theories of trauma identify the creation of a coherent trauma narrative and therapeutic exposure to trauma memories as potential recovery mechanisms. These factors are often inherent to the disclosure process, resulting in a parallel theoretical framework for experimental research that conceptualizes disclosure as a therapeutic intervention. The present investigation examined the moderational impact of disclosure following trauma on the link between trauma severity and symptoms of Posttraumatic Stress Disorder (PTSD). Disclosure status (discloser or nondiscloser), highest extent of disclosure, and length of delay to first disclosure were tested in a series of moderated regression models among a sample of female physical and sexual assault victims (N = 1087). Findings indicate that engaging in more detailed disclosure is associated with a modest beneficial impact on PTSD, but that the majority of nondisclosers have lower symptom levels than disclosers. There is also evidence for a small subset of nondisclosers that remain at heightened distress. A unique effect was found for disclosure delay, such that for physical assault, delaying disclosure is associated with a progressively weakening negative relation between time since the trauma and PTSD. At extreme delays, the association may become positive. Findings have implications for theories of trauma recovery and therapeutic interventions, including concerns about early interventions that emphasize disclosure. Future research may benefit from focusing on nondisclosing trauma victims to gain greater insight into recovery processes.
ContributorsFields, Briana (Author) / Barrera, Manuel (Thesis advisor) / Holtfreter, Kristy (Committee member) / Knight, George (Committee member) / Chassin, Laurie (Committee member) / Arizona State University (Publisher)
Created2010
Description
Post-Traumatic Stress Disorder (PTSD) is characterized by intrusive memories from a traumatic event. Current therapies rarely lead to complete remission. PTSD can be modeled in rodents using chronic stress (creating vulnerable phenotype) combined with fear conditioning (modeling a traumatic experience), resulting in attenuated extinction learning and impaired recall of extinction. Studies typically investigate cognition soon after chronic stress ends; however, as days and weeks pass (“rest” period) some cognitive functions may improve compared to soon after stress. Whether a rest period between chronic stress and fear conditioning/extinction would lead to improvements is unclear. In Chapter 2, male rats were chronically stressed by restraint (6hr/d/21d), a reliable method to produce cognitive changes, or assigned to a non-stressed control group (CON). After chronic stress ended, fear conditioning occurred within a day (STR-IMM), or after three (STR-R3) or six weeks (STR-R6). During the first three extinction trials, differences emerged in fear to the non-shock context: STR-R3/R6 showed significantly less fear to the context than did STR-IMM or CON. Differences were unlikely attributable to generalization or to second-order conditioning. Therefore, a rest period following chronic stress may lead to improved fear extinction and discrimination between the conditioned stimulus and environment. In Chapter 3, the infralimbic cortex (IL) was investigated due to the IL’s importance in fear extinction. Rats were infused with chemogenetics to target IL glutamatergic neurons and then assigned to CON, STR-IMM or STR-R3. During the rest period of STR-R3 and the restraint for STR-IMM, the IL was inhibited using CNO (1mg/kg BW, i.p., daily), which ended before behavioral testing. STR-R3 with IL inhibition failed to demonstrate a tone-shock association as spontaneous recovery was not observed. CON with IL inhibition behaved somewhat like STR-IMM; freezing to the extinction context was enhanced. Consequently, inhibiting IL function during the rest period following chronic stress was particularly disruptive for learning in STR-R3, impaired freezing to a safe context for CON, and had no effect in STR-IMM. These studies show that time since the end of chronic stress (recently ended or with a delay) can interact with IL functioning to modify fear learning and response.
ContributorsJudd, Jessica Michelle (Author) / Conrad, Cheryl D. (Thesis advisor) / Sanabria, Federico (Committee member) / Olive, Michael F (Committee member) / Bimonte-Nelson, Heather A. (Committee member) / Arizona State University (Publisher)
Created2020