Doctor of Philosophy, The Ohio State University, 2020, Social Work

Background: The unique recovery process and treatment needs of persons with bipolar II disorder (BD II) has been subject of limited research. BD II is associated with high rates of disability worldwide and people with BD II are among the highest risk of suicide of all populations. Research of psychotherapy for bipolar disorders (BDs) in general has focused on clinical outcomes (i.e., reducing mood symptoms, remission of mood episodes) rather than functional outcomes, suicide risk, or co-occurring problems. This dissertation addresses these gaps in three quantitative studies, which investigate the recovery process of individuals with BDs and what treatment (i.e., psychotherapy alone or in combination with medication) works for whom (i.e., individuals with childhood trauma, anxiety, and various stages of illness progression) to improve symptoms, reduce suicidal thoughts, and restore functioning to all major life areas. The goal of these studies is to inform treatment considerations for BD II to decrease the high rates of mortality and disability associated with BD II. These studies are guided by kindling theory and social rhythms disruption therapy, which emphasize stressful life events and disruption of social and biological rhythms, in combination with genetic predisposition to explain the etiology and ongoing expression of BDs. Methods: Study design consisted of a randomized, double blind, controlled trial (ClinicalTrials.gov identifier: NCT01133821) testing the efficacy of interpersonal social rhythms therapy (IPSRT) plus placebo compared to IPSRT plus medication (i.e., quetiapine) for adults with BD II depression (n = 92). Study 1 used multilevel logistic regression with growth curve modeling to examine (1) the comparative effectiveness of IPSRT plus placebo compared to IPSRT plus medication on suicidal ideation outcomes, and (2) whether higher levels of childhood trauma and anxiety predicted change in suicidal ideation. Study 2 used multilevel modeling with gro (open full item for complete abstract)

Committee: Theresa Early PhD (Committee Chair); Tamara Davis PhD (Committee Member); Alicia Bunger PhD (Committee Member); Natasha Slesnick PhD (Committee Member) Subjects: Medicine; Mental Health; Psychology; Psychotherapy; Social Work

PhD, University of Cincinnati, 2014, Medicine: Neuroscience/Medical Science Scholars Interdisciplinary

An estimated 35 million diabetic patients worldwide take antipsychotic medications for a variety of co-morbid mental illnesses. Diabetic patients frequently experience hypoglycemic episodes ranging from mild to severe. Interestingly, the combination of antipsychotic medications and hypoglycemia has remained largely unstudied. Both antipsychotic medications and hypoglycemia modulate extracellular glutamate creating the potential for glutamate-mediated excitotoxicity. The typical antipsychotic medication, haloperidol, has been shown to elevate extracellular glutamate levels through its binding pharmacology at the D2 and 5HT1A receptors. Conversely, quetiapine, an atypical antipsychotic medication, is not predicted to elevate extracellular glutamate through its binding pharmacology at the D2, 5HT1A, and 5HT2A receptors and may be less likely to induce this toxicity when combined with hypoglycemia. We hypothesized that haloperidol and hypoglycemia, not quetiapine and hypoglycemia, would elevate neuronal death and microglial activation. We predicted that this would occur through glutamate-mediated excitotoxicity potentiated by activated microglia. We investigated this hypothesis by combining these medications with a range of different hypoglycemic episodes: acute, severe; single, moderate; and multiple, moderate. The combination of severe hypoglycemia with these antipsychotic medications showed that both medications elevated neuronal death as compared to hypoglycemia alone. This suggests that the predicted abilities of quetiapine to attenuate extracellular glutamate levels and prevent glutamate-mediated excitotoxicity of neurons are overshadowed in instances of severe hypoglycemia. However, when moderate hypoglycemic episodes were combined with antipsychotic medications, no changes in neuronal death or microglial activation were detected. Overall, these data suggest that severe hypoglycemia and antipsychotic medications induce neuronal death, but the effect (open full item for complete abstract)

Committee: Gary Gudelsky Ph.D. (Committee Chair); Steve Danzer Ph.D. (Committee Member); Andreas Loepke M.D.Ph.D. (Committee Member); Neil Richtand M.D. (Committee Member); Renu Sah Ph.D. (Committee Member) Subjects: Neurology