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Hur, Cem. "Tackling Bipolar Disorder." Thesis, Birmingham City University, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.731716.
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Knowles, Rebecca Elizabeth. "Psychology of bipolar disorder." Thesis, University of Manchester, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488262.
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A behavioural high risk paradigm was used to investigate cognitive vulnerability to bipolar disorder in a group of individuals at high risk of developing symptoms, and similar measures were administered to a group of bipolar patients whose symptoms were currently in remission. High risk was defined as a combination of elevated scores on both the Hypomanic Personality Questionnaire and the Dysfunctional Attitudes Scale. The research addressed several psychological models of bipolar disorder including response styles, behavioural engagement, circadian rhythm disruption, self-esteem instability and the manic defence, as well as cognitive reactivity to musical mood induction and the impact of mood on emotion recognition. In the initial analogue study, hypothetically low-, medium- and high-risk participants were compared on measures of the models listed. High-risk participants displayed a uniquely dysfunctional combination of rumination and risk-taking coping behaviours, high behavioural inhibition and activation scores, irregular and unrestful sleep, highly unstable self-esteem, heightened sensitivity to positive and negative mood induction, and a moodcongruent bias in their perception of ambiguous facial expressions relative to the low-risk participants. They had also experienced significant levels of affective symptomatology consistent with their high-risk status. The subsequent clinical study compared remitted bipolar patients to remitted unipolar depressed patients and healthy controls. The bipolar group displayed more ruminative coping, high behavioural inhibition, disrupted and inefficient sleep, unstable selfesteem, and a clear manic defence when compared to the controls. The remitted bipolar patients also reported greater shifts in mood and self-esteem following both mood induction procedures than the controls. The remitted bipolar patients were therefore very similar to both the unipolar depressed group and the high-risk analogue participants in cognitive terms. Taken together, the results support the use of behavioural high-risk paradigms in investigations of bipolar disorder, and confirm the involvement of the presently examined cognitive and psychosocial factors in conferring vulnerability to bipolar symptomatology.
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Ortiz-Dominguez, Tania Abigail. "Migraine comorbidity in bipolar disorder." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116105.
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Introduction: Bipolar Disorder (BD) is a chronic mental illness associated with functional decline, mortality, and significant health care costs; furthermore, specific general medical conditions have been found to occur disproportionately within BD patient populations, among them, migraine is one of the most studied. Migraine has a global prevalence of 10%, and it is a disorder with elevated direct and indirect costs, the later mostly derived from its association with mood and anxiety disorders. Specifically, the reported prevalence of migraine in the BD population ranges from 24.8% to 39.8%, rates that are considerable higher than those found in the general population.Objective: To explore the prevalence and clinical characteristics of BD patients with and without migraine (Study 1), and to examine the psychiatric comorbidity in patients suffering from migraine (Study 2).
Methods: 323 BD patients were studied, using SADS-L and SCID as diagnostic interviews, and ill-Migraine questionnaire to assess the presence of migraine. Statistical analyses were conducted using parametric analysis and the development of log-linear models. Additionally, 102 migraine patients were interviewed using SADS-L, and the descriptive characteristics of the sample were analyzed.
Results: For Study 1, we found that 24.5% of BD patients suffer from migraine, and it is significantly associated with BD 2, suicidal behaviour, and a variety of anxiety disorders. As well, over 70% of migraine patients showed a lifetime psychiatric diagnosis, mainly within the spheres of mood and anxiety disorders; specifically, the prevalence of BD among migraine patients was 12.7%.
Conclusions: Our study highlights the high prevalence of migraine among BD patients, and the elevated prevalence of psychiatric comorbidity among migraine sufferers. The study of this comorbidity will deepen our understanding of the mechanisms that underlie both disorders and provide a better framework for the developing of molecular techniques to further analyze the molecular physiopathology of Bipolar Disorder.
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Hillegers, Manon Hubertine Johanna. "Developing bipolar disorder a follow-up study among children of patients with bipolar disorder /." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2007. http://irs.ub.rug.nl/ppn/301812861.
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Sobczak, Sjacko. "Serotonin and bipolar disorders serotonergic vulnerability in first-degree relatives of patients with bipolar disorder /." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 2002. http://arno.unimaas.nl/show.cgi?fid=7073.
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Chabler, Leslie Anne. "Familial factors in bipolar disorder." Connect to resource, 1987. http://rave.ohiolink.edu/etdc/view.cgi?acc%5Fnum=osu1244209127.
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Clark, Luke. "Neuropsychological investigations in bipolar disorder." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368012.
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Cole, Sarah. "Risk taking in bipolar disorder." Thesis, University of Hull, 2009. http://hydra.hull.ac.uk/resources/hull:2400.
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Part 1 Background: People with a diagnosis of bipolar disorder can make suboptimal decisions during manic and depressive episodes which can have negative long-term consequences. This review aims to explore individual factors, including mood state and personality traits, which could affect decision making processes of individuals with bipolar disorder. Methods: A systematic search of three databases, plus hand searching relevant reference sections, identified twenty five relevant studies, nineteen of which met the inclusion criteria for the review. Results: Mania and severe depression are associated with poorer performance on computerised tasks designed to measure risk decision making. There is tentative evidence for altered decision making processes even during euthymic and remitted phases of bipolar disorder, but little difference in overall decision making outcomes. Limitations: The evidence base is small and centred around a few computerised tasks, which may have limited ecological validity in the assessment of decision making. Complex decision making tasks are difficult to interpret in terms of underlying processes. Conclusions: Both mood episode and trait factors, such as impulsivity, may have some predictive value of decision making in people with a diagnosis of bipolar disorder, although trait factors are largely unexplored in this population. Further research is needed to develop a psychological model for understanding the relative impact of individual factors, plus social and environmental factors which can influence the decision making process. Part 2 "Excessive" risk taking behaviour is a clinical characteristic of a manic episode, which can lead to harmful consequences for the individual with bipolar disorder. This study investigated the hypothesis that risk taking behaviour may be more sensitive to change following mood induction in people with bipolar disorder than in controls. Participants were 26 people with bipolar I disorder who were out of an acute episode and 28 healthy controls. Risk taking was measured using the Balloon Analogue Risk Task (BART; Lejuez et al, 2002), a computerised task that has been found to correlate with real world risky behaviours. After baseline measures, participants were randomly assigned positive or negative mood induction and completed two sets of BART trials, before and after mood induction. Trait sensitivity to reward was also measured, as a potential factor underlying BART performance. The primary hypothesis was not supported by the findings, nor could the variance in risk taking before or after mood induction be explained by trait sensitivity to the behavioural activation system. The bipolar group demonstrated less risk taking at baseline than controls. The results suggest excessive risk taking behaviour may be specifically associated with manic symptoms other than positive affect. However people with bipolar disorder may make poorer quality risk decisions out of an acute episode than controls.
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Smith, Angela Mary. "Psychological Processes in Bipolar Disorder." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492751.
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The present research addressed several diathesis models of bipolar disorder including Behavioural Activation, stress sensitivity and circadian rhythm disruption and considered cognitive vulnerability factors such as self-esteem and affective instability, response styles to depression and depressogenic cognitive styles. These relationships were examined prospectively in healthy controls, remitted unipolar patients and bipolar disorder participants who were remitted, depressed or hypomanic.
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Taylor, Jayne Louise. "Self-representations in bipolar disorder." Thesis, University of Leeds, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416487.
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NASCIMENTO, RODRIGO LEAO FERREIRA DO. "IMPLICIT INSIGHT INTO BIPOLAR DISORDER." PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIRO, 2018. http://www.maxwell.vrac.puc-rio.br/Busca_etds.php?strSecao=resultado&nrSeq=34485@1.
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PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIROCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO
Prejuízo de insight costuma ser reportado no Transtono Bipolar (TB), sobretudo quando os pacientes viram para o pólo maníaco do transtorno. Essa falha na consciência verbal dos déficits, sinais e sintomas do transtorno pode vir acompanhada de uma forma de insight implícito, que é a demonstração indireta de algum nível de conhecimento sobre a doença ou uma deficiência com perda parcial ou total de reconhecimento verbal. Dois estudos foram conduzidos para verificar as relações entre as formas de insight explícito e implícito no TB. Para isso, foi utilizado um modelo teórico conhecido como The Cognitive Awareness Model (CAM), que permite investigar dissociações nos padrões de consciência implícita e explícita. No primeiro estudo, os participantes foram avaliados em relação à uma série de variáveis clínicas, incluindo uma medida de insight explícito, além de uma medida de insight implícito com estímulos ligados à depressão e à mania. No segundo estudo, os participantes foram igualmente testados em relação às variáveis clinicas, incluindo uma medida de insight explícito, além de uma medida de insight implícito com estímulos ligados à condição de saudável e doente. Os resultados de ambos os estudos apontaram para diferenças nas medidas de insight explícito entre os grupos de maníacos e eutímicos, e demonstraram diferenças no tempo médio de reação para auto-associações implícitas para condição. A partir desses resultados, pode-se sugerir que os pacientes em mania se autoavaliam explicitamente de forma similar aos pacientes em eutimia, o que pode trazer prejuízos na adesão ao tratamento, ao passo que os pacientes bipolares apresentaram uma forma de insight implícito tanto para os sintomas quanto para a condição de doente avaliadas.
Lack of insight is usually reported in Bipolar Disorder (TB), especially when patients have seen the manic pole of the disorder. This lack of verbal awareness of deficits, signs and symptoms of the disorder may be accompanied by an implicit insight, which is the indirect demonstration of some level of knowledge about the disease or a disability with partial or total loss of verbal recognition. Two studies were conducted to verify the relationships between explicit and implicit forms of insight into TB. For this, a theoretical model known as The Cognitive Awareness Model (CAM) was used, which allows to investigate dissociations in the patterns of implicit and explicit consciousness. In the first study, participants were assessed for a number of clinical variables, including an explicit insight measure, as well as an implicit insight measure with depression and mania-related stimuli. In the second study, participants were also tested for clinical variables, including an explicit insight measure, as well as an implicit insight measure with stimuli linked to healthy and ill status. The results of both studies pointed to differences in measures of explicit insight between the manic and euthymic groups and demonstrated differences in mean reaction time for implied self-associations for condition. From these results, it can be suggested that patients in mania explicitly self-evaluate in a similar way to patients in euthymia, which can lead to impairment in adherence to treatment, whereas bipolar patients presented an implicit insight for symptoms and for the patient s condition evaluated.
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Kandaswamy, R. "Molecular genetics of bipolar disorder." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1370613/.
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Bipolar affective disorder has a strong genetic heritability. In the UCL laboratory, a locus on chromosome 1p36 was found to be linked to bipolar and related unipolar affective disorders with a log of the odds score above 3.00. This region was subjected to fine mapping using tests of allelic association in a case-control sample as part of this thesis in order to identify the genes involved in bipolar disorder. In addition, a GWAS was also employed to fine map other bipolar affective disorder susceptibility genes. The tests of allelic association found evidence for the involvement of the PRKCZ gene. Markers D1S243 and rs3128396 at the PRKCZ gene were significantly associated with bipolar disorder with empirical P = 0.037 and P = 0.040, respectively. Other loci encoding brain expressed proteins found to be associated in the UCL GWAS sample were the genes - GRM3 and GRM7. Therefore, these genes were sequenced using PCR-based genomic sequencing. A 3'-UTR base pair change (rs56173829) in the GRM7 gene was found to be significantly associated with the disorder, although the minor allele was more frequent in controls. A base pair mutation (rs148754219) was found in the GRM3 exon 1 two bases before the translation start codon (forming part of Kozak sequence) of a GRM3 receptor isoform. The mutation was associated with bipolar disorder (P = 0.0046, odds ratio 4.2 (95% CI 1.42-12.37)). Transcription factor binding assays and cloning experiments comparing the gene expression activity of wild-type and mutant alleles showed that the mutant allele strongly affected the reporter gene activity in SH-SY5Y and HEK293 cells. If the GRM3 Kozak sequence mutation is confirmed as an important mutation in the aetiology of bipolar disorder, then it could be used as a marker for personalised treatment for a genetic subtype of affective disorders.
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Rock, Philippa L. "Emotional processing and bipolar disorder." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:f4a311fe-3bda-40cc-852a-11dbde8f436c.
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The aetiology of bipolar disorder remains unclear and investigation to date has focussed largely on bipolar patients. Whilst ultimately of huge value, such studies may also be confounded by current mood or experience of repeated illness episodes or current or past medication; using at-risk samples may bypass some of these problems. The current research therefore assessed the efficacy of the Mood Disorder Questionnaire (MDQ) as a screening tool for vulnerability to bipolar disorder. The MDQ was used with two sets of criteria to identify two sub-groups of medication-naïve young bipolar phenotype subjects who were at risk for bipolar disorder by virtue of experience of mood elevation. Analysis of data from the Student Stress Survey was carried out to characterise the bipolar phenotype. Compared to a control group with no experience of mood elevation, the two bipolar phenotype sub-groups showed a gradient of prevalence of bipolar diagnosis and associated co-morbidity. Behavioural and functional magnetic resonance imaging (fMRI) techniques were employed to investigate emotional processing, decision-making, and sleep and circadian rhythmicity in bipolar phenotype students. Analyses revealed that positive emotional processing biases, disrupted decision-making, and increased activity during sleep were associated with the bipolar phenotype and, therefore, may represent vulnerability markers for bipolar disorder. Finally, a psychopharmacological investigation of quetiapine, which stabilises mood, was carried out in healthy volunteers. One-week quetiapine administration resulted in biases away from both positive and negative emotional stimuli (i.e. a mood-stabilising effect), reduced discrimination between different magnitudes of gains and losses during risky decision-making (consistent with an antidepressant effect), and increased sleep duration. In sum, this research has developed our understanding of vulnerability markers associated with the bipolar phenotype and provided a first step towards uncovering the psychological mechanisms through which quetiapine’s clinical effects may be mediated.
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Weathers, Judah D. "Cognitive functioning in bipolar disorder." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:6a73683c-0047-4285-a251-2414a0f64d0f.
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To align the neuropsychological functioning of our adult euthymic patient group with that reported in previous studies on euthymic bipolar disorder (BD), we used a neuropsychological battery that examined sustained attention (Rapid Visual Information Processing Task), verbal memory (California Verbal Learning Task), executive functioning (Intradimensional-Extradimensional Shift Task, Barrett Impulsivity Task, and Framing Task), and emotion responsiveness/regulation (Positive Affect/Negative Affect Scales, Behavioral Inhibition/Behavioral Activation Scale, and Affective Lability/Affective Intensity Scales) in patients versus healthy volunteers (HV). Our results corroborated existing evidence of reduced sustained attention, impaired verbal memory and executive functioning, and abnormal emotional responsiveness and regulation in euthymic BD relative to healthy controls (Chapter 2). To investigate how abnormal development of brain function in BD leads to deficits in decision-making, motor inhibition, and response flexibility, we examined child and adult BD using a novel risky decision-making task, and used cross-sectional (age x diagnosis) functional magnetic resonance (fMRI) designs to examine neural activation associated with motor inhibition and response flexibility in BD relative to HV. During the risky decision-making task, adult euthymic BD patients were no different from healthy controls in their proportion of risky lottery choices over a range of competing lotteries. This matched behavioral performance was associated with similar prefrontal and striatal brain activation between the patient and control groups during response, anticipation, and outcome phases of decision-making (Chapter 3). These results are different from previous studies that have shown increased risk taking during decision-making in euthymic BD. Similarly, young BD patients were no different from age-matched healthy and patient controls in their pattern of decision making during the risky choice task. This was evidenced by a similar number of risky lottery selections over the range of changing expected values between the young BD group and control groups (Chapter 4). Using a cross-sectional, fMRI analytic design during the stop signal task, we found that child and adult BD showed similar behavioral performance to child and adult HV during motor inhibition. However, this matched behavioral performance was associated with abnormal neural activation in patients relative to controls. Specifically, during unsuccessful motor inhibition, there was an age group x diagnosis interaction, with BD youth showing reduced activity in left and right ACC compared to both age-matched HV and adult BD, and adult BD showing increased activation in left ACC compared to healthy adults. During successful motor inhibition there was a main effect of diagnosis, with HV showing greater activity in left VPFC and right NAc compared to BD (Chapter 5). These neuroimaging data support existing laboratory-based evidence of motor inhibition impairments in BD relative to HV, and indicate brain dysregulation during motor control is important to BD pathophysiology. A previous behavioral study showed impaired response flexibility in young BD patients relative to age-matched controls when using the change task. Here, we used the change task during fMRI to examine response flexibility in child and adult BD compared to child and adult HV. We found that patient and control groups showed similar change signal reaction times in response to change cues. However, this matched behavioral performance was associated with abnormal age group x diagnosis activations in brain regions important in signal detection, response conflict, response inhibition, and sustained attention. Specifically, during successful change trials, child BD participants showed frontal, parietal, and temporal hyperactivation relative to healthy children and adult BD, while adult BD showed hypoactivation in these regions relative to healthy adults. These novel fMRI findings during the change task indicate impaired neural activation during response flexibility may be important to the pathophysiology of BD development.
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LEBOWITZ, BRIAN K. "INHIBITORY CONTROL IN BIPOLAR DISORDER." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1093016997.
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Pavlickova, Hana. "Psychological vulnerability in bipolar disorder." Thesis, Bangor University, 2013. https://research.bangor.ac.uk/portal/en/theses/psychological-vulnerability-in-bipolar-disorder(7a7c7ece-e279-4477-93f8-046c035dc500).html.
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Background: The current understanding of bipolar disorder attributes a causal role to abnorma1 psychological processes in its development. However, little research has so far adequately tested this assumption. Two approaches might be employed to do so: (i) longitudinal investigations of psychological processes in patients (with some limitations); (ii) examinations of such processes in high-risk individuals. Methods: Three cohorts of participants were examined: two different cohorts of adults with bipolar disorder (using secondary data, Chapter 2 and 3), and adolescent offspring of parents with bipolar disorder, in comparison to offspring of control parents (Chapters 4, 5, 6). In adults with bipolar disorder, the associations between self-referential processes and symptoms of depression and mania (Chapter 2), and the inter-relationship between self-esteem, mood and response styles (Chapter 3) were examined longitudinally. In adolescent children, longitudinal relationship between mood, self-esteem and coping style (Chapter 4), abnormal psychological processes (Chapter 5), and explicit and implicit self-esteem and their discrepancies (Chapter 6), were investigated. Results: In adults with bipolar disorder, symptoms of depression and mania were associated with distinct psychological processes, with self-esteem being the most robust predictor (Chapter 2). However, mood, rather than self-esteem, instigated, and was affected by, an engagement in coping strategies (Chapter 3). In adolescents, index adolescents showed compromised capacity to employ adaptive coping, and employed risktaking in response to low self-esteem (Chapter 4). Further, no differences in abnormal psychological processes were found, unless children have already met diagnostic criteria for psychiatric disorders (Chapter 5). Despite no differences in explicit and implicit self-esteem, index offspring reported marginally higher level of self-esteem discrepancies. In addition, damaged self-esteem (i.e. low explicit self-esteem and high implicit self-esteem) was related to symptoms of depression, whilst low implicit self-esteem to symptoms of mania. Conclusions: Early coping abnormalities are important markers of individuals at ultra high lisk of bipolar disorder. Further, the relevance of self-esteem in bipolar disorder has been suggested. Implications for future research and psychotherapy are discussed.
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Dalvie, Shareefa. "Genetic analysis of bipolar disorder and alcohol use disorder." Doctoral thesis, University of Cape Town, 2015. http://hdl.handle.net/11427/16560.
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Includes bibliographical referencesBackground: Mental health disorders represent a major public health problem in most countries around the world. In South Africa, the lifetime prevalence of psychiatric disorders is 30.3%, with substance-use disorders and mood disorders being the second and third most prevalent classes of lifetime disorders, respectively. Bipolar disorder (BD) has a lifetime prevalence of 1.4% and alcohol use disorder (AUD) a lifetime prevalence of 30.3%, and they are frequently comorbid. Both of these disorders have a relatively high heritability, yet the exact genetic basis of each remains unknown. Genetic variants within the hypothalamic-pituitary-adrenal (HPA)-axis and glutamatergic pathways have previously been implicated in both phenotypes. The aim of this project was to investigate the aetiology of BD and AUD, using high-throughput genomic technologies, bioinformatics, brain-imaging and environmental measures. An additional aim was to assess the genetic aetiology of BD-AUD comorbidity. Methods: For the genetic analysis underlying BD, a South African 'Afrikaner' family was investigated. Whole-genome sequencing (WGS) and whole-genome linkage analysis was performed for individuals with BD Type I (BDI) and unaffected family members using the Illumina HiSeq2000 and Affymetrix Axiom TM Genome-wide CEU 1 Array, respectively. For the AUD analysis, two groups were investigated; a South African adolescent group comprising 80 individuals with AUD and 80 controls, and a group of 8123 individuals from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort. The South African group of adolescents were genotyped using the Illumina Infinium iSelect custom 6000 BeadChip, childhood trauma data was obtained and brain magnetic resonance images were collected for a subset of this group. Genotype data on HPA-axis genes were obtained from a previous study for the ALSPAC cohort. The fourth group of individuals investigated in this thesis comprised 233 individuals with BD-AUD comorbidity from the Systemic Treatment Enhancement Program for BD (STEP-BD). Genotype data for genes from the glutamatergic and HPA-axis pathways were obtained from a previous study conducted on these individuals. Results: The chromosomal regions 6p25, 10p14-10p15.1, 11q23-11q25, and 13q21-22 scored the highest LOD scores for BD and the most over-represented pathway in the affected family members was the T-cell receptor signalling pathway. In the South African adolescent group, circadian rhythm genes were associated with AUD and childhood trauma predicted alcohol use in adolescence. The gene-imaging analysis identified a SNP in the glutamate receptor, ionotropic, N-methyl D-aspartate 2B (GRIN2B) gene as being associated with brain volume in the left orbitofrontal cortex and posterior cingulate. HPA-axis genes did not show an association with AUD and no significant gene x environment interactions were detected for AUD in the ALSPAC cohort. Single variants in the glutamatergic genes and HPA-axis were not associated with BD-AUD comorbidity. However, from the gene-based analysis, the glutamatergic gene PRKCI was associated with BD-AUD comorbidity. Conclusions: It appears that disruption in immune-related genes may contribute to the development of BD in an Afrikaner family. No significant gene x environment interactions were detected for adolescent AUD. The circadian pathway and childhood trauma may play a role in the development of adolescent AUD. Differential brain volume and BD-AUD comorbidity may be characterised by variation in the glutamatergic pathway. These pathways and the interactions between them should be further investigated in BD and AUD.
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McCabe, Patrick J. "Cannabis Use and Bipolar Disorder: Bipolar Disorder Case Identification and Cannabis Use Risk Assessment: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/584.
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Bipolar disorders (BD) are characterized by symptoms of grandiosity, decreased need for sleep, pressure to keep talking, flight of ideas, distractibility, increased goal-directed activities, psychomotor agitation, and excessive involvement in pleasurable activities. Those with a bipolar disorder have a high degree of psychiatric comorbidity including substance use disorders, and they also experience increased mortality. Despite the widespread recognition of BD as an important psychiatric condition, available population-based estimates for BD prevalence differs across data sources.
Cannabis is one of the most widely-used illicit substances. Evidence supports it as a risk factor for psychotic symptoms and disorders. Because populations with psychotic disorders and populations with bipolar disorder share genetic characteristics, cannabis may increase risk for bipolar disorders through the same pathways as it does with psychotic disorders. Limited and conflicting evidence regarding the association of cannabis use and bipolar disorder is currently available. This dissertation investigates cannabis use as a risk factor for incident manic symptoms and bipolar disorders in a large nationally representative longitudinal cohort.
The first aim of this dissertation is to evaluate the implications for manic, hypomanic and major depressive episode prevalence estimates arising from the different approaches to assessing DSM-IV criterion between two national surveys. Differences in the assessment of impairment strongly influence manic or hypomanic classification within the NESARC. Compared to multiple imputation estimates (19.7% [95% CI: 19.3-20.1]) which treat depressed mood and anhedonia as separate symptoms, symptom assessment in the NESARC substantially underestimates major depressive episode prevalence (16.9% [95% CI: 16.1-17.6]).
The second research objective examined self-reported cannabis use as a risk factor for incident manic symptoms, bipolar spectrum disorders (including manic and hypomanic episodes) and SCID-based recalibrated BD I and II. Cannabis use risk was assessed in the population as a whole and in sub-populations defined by age, substance abuse/dependence status, and family history. Among those reporting no lifetime major depressive or manic symptoms at baseline, self-reported past-year cannabis use was associated with increased odds of an incident week of extremely elevated or irritable mood accompanied by at least two manic episode criterion B symptoms (adj. OR 1.69, 95% CI: 1.08-2.65, p=.02) over the three year follow-up period. Among adults (ages 26 to 45) >=1 reported use(s) of cannabis per week was associated with incident manic or hypomanic episodes (adjusted OR 2.52, 95% CI: 1.32-4.80, p=.006). Among those endorsing no major depressive symptoms, substance abuse/dependence, or anti-social traits in their first degree relatives, past year cannabis use is associated with increased risk for incident bipolar spectrum disorders (adjusted OR 2.27, 95% CI: 1.01-5.10, p=.05) and CIDI recalibrated BD I and II (adjusted OR 5.49, 95% CI: 1.38-21.9, p=.02). Past year cannabis use risk for DSM-IV manic or hypomanic episodes among those aged 26 to 45 is concentrated in those with a baseline history of a substance use disorder (adj. OR 2.00, 95% CI: 1.10-3.66, p=.02) as compared to those with no such history (adj. OR 1.87, 95% CI: 0.49-7.21, p=.36).
The third research objective of this dissertation was a sensitivity analysis using externally-predicted categorized exposures and continuous cannabis use propensities. The sensitivity analysis found evidence of exposure misclassification. Exposures defined by external propensity scores had improved cross-sectional association with bipolar spectrum disorders compared to reported use when both were compared to an external standard. No significant risk estimates were found for categorized predicted cannabis use among groups that were previously found to have significant risk from reported exposure. However, among adults 18 to 45 years of age with no manic or major depressive symptoms at baseline, past year cannabis use propensity (as a log transformed continuous measure) was associated with incident manic or hypomanic episodes (adj. OR 1.49, 95% CI: 1.10-2.03, p=.01). Elevated risk for high cannabis use propensity (>=1 use/week in the past year) was also found in this same group (adj. OR 1.33, 95% CI: 1.03-1.72, p=.03). Among those with no reported history of depression, substance abuse/dependence, or anti-social traits among their first-degree relatives, propensity for past year cannabis use (adj. OR 1.61, 95% CI: 1.11-2.32, p=.01) and propensity for >=1 use/week of cannabis in the past year (adj. OR 1.38, 95% CI: 1.03-1.85, p=.03) were associated with incident manic or hypomanic episodes. Among those without a substance use history at baseline, propensity for past year cannabis use (adj. OR 1.63, 95% CI: 1.33-1.55, p=1 use/week of cannabis in the past year (adj. OR 1.54, 95% CI: 1.26-1.88, p
The findings of the first aim support the conclusion that the AUDADIS substantially under-estimated lifetime major depressive episode prevalence compared to an imputed estimate that treated anhedonia and depressed mood as separate and concurrent MDE symptoms. The operationalization of impairment for manic disorders in both the AUDADIS and CIDI strongly influences case identification, with the CIDI having suppressed manic and hypomanic prevalence estimates. Evidence was found supporting the conclusion that self-reported cannabis use is a significant risk factor for incident bipolar spectrum outcomes within subpopulations in a nationally representative cohort. A sensitivity analysis finds evidence that supports the conclusion that increasing cannabis use propensity is associated with increased risk of bipolar spectrum outcomes within population subgroups, with the greatest increased risk among those with the lowest innate risk. Under-reporting of illicit substance use is a major limitation in this dissertation; further study is needed with improved exposure measures.
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Healy, Helen G. "Cognition and emotion in bipolar disorder." Thesis, Bangor University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417222.
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Grozeva, Detelina. "Copy number variation in bipolar disorder." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54197/.
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A plethora of studies have suggested that copy number variation in the human genome is extensive and may play an important role in susceptibility to disease, including neuropsychiatric disorders such as schizophrenia and autism. The possible involvement of copy number variants (CNVs) in bipolar disorder has received little attention to date. This PhD thesis describes work that sought to determine whether large (≥ 100 kb) and rare (with frequency ≤ 1%) CNVs are associated with susceptibility to bipolar disorder and to make comparisons with previous findings in schizophrenia. In order to do that, a genome-wide survey of large and rare CNVs in a case-control sample using a high-density microarray was performed. 1697 cases of bipolar disorder and 2806 non-psychiatric controls were genotyped using Affymetrix 500K array set. Subsequently, the copy number data were inferred and analysed. The burden of CNVs in bipolar disorder was not increased compared with controls. Furthermore, CNVs > 1 Mb were found with statistically significant lower rate in bipolar disorder as compared to schizophrenia. In addition, CNV loci previously implicated in the aetiology of schizophrenia were not more common in cases with bipolar disorder. The main observation was that large and rare CNVs do not have a major effect in the susceptibility to bipolar disorder. In addition, it was noted that bipolar disorder and schizophrenia differ with respect to CNV burden in general and specific CNVs in particular. As the same CNVs implicated in schizophrenia, have been observed in autism and mental retardation, and not in bipolar disorder, it is reasonable to postulate that CNVs could be a specific genetic factor for a predisposition to disorders with stronger neurodevelopmental component than bipolar disorder. This study has provided one of the first glimpses of the possible involvement of copy number variation in the susceptibility to bipolar disorder.
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McAuley, Erica Zoe Prince of Wales Medical Research Institute Faculty of Medicine UNSW. "Identification of bipolar disorder susceptibility genes." Publisher:University of New South Wales. Prince of Wales Medical Research Institute, 2009. http://handle.unsw.edu.au/1959.4/43690.
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Bipolar affective disorder is a severe mood disorder, which is characterised by episodes of mania and depression. The aetiology of bipolar disorder remains elusive, with little known about the underlying biological, anatomical, or biochemical effects. However, family, twin and adoption studies provide evidence for a strong genetic component to the disorder. Due to the high heritability, familial clustering, and common population prevalence of the illness, molecular genetic studies can be implemented to identify bipolar disorder susceptibility genes. This thesis investigated the candidate gene serotonin 2A receptor (HTR2A), which lay within a region on chromosome 13q14 previously identified by bipolar disorder genome-wide linkage scans. Significant association was found with bipolar disorder and a SNP within intron 2 of HTR2A in an Australian case-control cohort. Haplotype association analysis identified a 5-SNP protective haplotype within HTR2A. Conducting a new genome-wide linkage scan on 35 Australian bipolar disorder pedigrees found significant evidence for linkage on chromosome 15q25-26. Subsequent fine-mapping of the region verified the linkage peak with a significant maximum multipoint LOD score of 4.58. Haplotype analysis, based on pedigree-specific, identical-by-descent allele sharing, supported the location of a bipolar susceptibility gene within a 6.2Mb confidence interval. The candidate gene sialyltransferase 8B (ST8SIA2), which had previously shown association with SNPs within the genes promoter region and schizophrenia in two independent Asian cohorts, lies within the chromosome 15q25-26 locus. Failing to replicate the association found with these specific SNPs, and without finding association with two additional SNPs in an upstream conserved putative regulatory region, a fine-mapping association study was conducted across the entire 6.2Mb interval. The strongest association signals were observed at SNPs 16kb upstream from and within the fourth intron of ST8SIA2. A specific bipolar disorder risk haplotype was identified for ST8SIA2, and this was also observed to be over-represented in a cohort of Australian schizophrenia cases. This finding suggests that the ST8SIA2 gene, for which strong developmental regulation was observed, may be a shared susceptibility gene for both bipolar disorder and schizophrenia. In summary, this thesis has provided evidence identifying both HTR2A and ST8SIA2 as bipolar disorder susceptibility genes.
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Bass, Nicholas James. "Genetic association studies of bipolar disorder." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444258/.
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Bipolar disorder is a common and serious mental illness. The occurrence of mania is central to the diagnosis, but affected individuals typically also suffer episodes of depression. The results of family, twin and adoption studies argue convincingly for genetic susceptibility to bipolar disorder. Linkage studies conducted at the Molecular Psychiatry Laboratory, UCL have previously implicated the regions 12q24, 21q22, lq42 and 11 pi4- 15 as harbouring susceptibly loci for bipolar disorder. In this thesis I report fine mapping of the 12q24, 21q22 and lq42 regions by linkage disequilibrium methods, employing a case-control design. For the llpl4-15 region association with the candidate gene BDNF was tested. I also present attempts to replicate findings of association at the genes DAOA and COMT, located in regions implicated by meta-analysis of the linkage data. I have attempted to put these investigations in context, necessitating consideration of the conceptual developmental of bipolar disorder, the classical techniques for assessing the genetic contribution to aetiology, and mapping strategies. Fine mapping of the UCL linkage regions implicated two novel susceptibility loci and provided support for two previously identified loci. Association of multiple markers within a 180 kb region of 12q24.3 was found, implicating Slynar and LOC387895. Association was also found with two markers in the more centromeric gene P2RX7, previously implicated in a Canadian sample. Multiple associated markers were found on 21q22.3. Two candidate genes - C21orf29 and TRPM2 - were identified from this region. Initial efforts to fine map the lq42 region suggested the involvement of the previously implicated DISCI gene. However association was only found with a single marker. Although haplotypic association was found with BDNF, the complex structure of the microsatellite marker hindered interpretation of the results. Partial replication of the association with DAOA was achieved but the involvement of COMT was not supported.
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Babiker, Nathan T. "Reward-oriented processes in bipolar disorder." Thesis, University of Hull, 2008. http://hydra.hull.ac.uk/resources/hull:1591.
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There is thought to be a link between characteristic reward-oriented processes in bipolar disorder and dysregulation in the behavioural activation system (BAS). This study aimed to assess differences between bipolar and healthy control individuals in their response to reward, failure and a reasoning task sensitive to data-gathering biases. Participants were 25 adults with bipolar I disorder and 25 healthy controls. Measures of sensitivity to reward and failure were collected during the first task (Go task), which included visual analogue ratings of mood and success expectancy, reaction time of button-pressing, and the difficulty level set by the participant. There were no significant differences between groups following reward feedback or failure feedback on the Go task. Results from the second task showed that bipolar individuals needed less data than controls before making a decision on the emotionally-neutral, difficult version of the task. The results are discussed in relation to current trends in bipolar research.
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Thompson, Jill Maria. "Cognitive architecture in euthymic bipolar disorder." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417560.
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El-Badri, Selim Mohamed. "Neurobiological changes in bipolar affective disorder." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242439.
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Joseph, Megan F. Youngstrom Eric Arden. "Cognitive performance in pediatric bipolar disorder." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,2064.
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Thesis (M.A.)--University of North Carolina at Chapel Hill, 2007.Title from electronic title page (viewed Feb. 17, 2009). "... in partial fulfillment of the requirements for the degree of Master of Arts in the Department of Psychology Clinical Psychology." Discipline: Psychology; Department/School: Psychology.
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Verdolini, Norma. "Self and Hetero-Aggression: Clinical Implications in Bipolar Disorder and Mixed States." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/665442.
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The poorest outcomes in bipolar disorder are represented by self-aggressive (i.e. deliberate self-harm, attempted or completed suicide) and hetero-aggressive violent behaviors. A better understanding of the clinical factors associated with both the risk of criminal behavior and the risk of self-injurious behaviors among individuals suffering from bipolar disorder may improve the course of illness and the risk management. The main objective of this doctoral thesis was to evaluate the psychiatric correlates of self- or hetero-aggression in the context of bipolar disorder, particularly in those patients presenting mixed features. The five published articles included in this thesis had different study designs: Study I. A meta-analysis including studies on the association between bipolar disorder and violent criminal behaviors; Study II. A cross-sectional study assessing clinical correlates of deliberate self-harm and suicide attempts in prisoners, particularly mood disorders and bipolar disorder; Study III. A post-hoc analysis of the Bipolar Disorders: Improving Diagnosis, Guidance and Education (BRIDGE)-II-MIX multicentric study aimed at evaluating hetero-aggression as a mixed feature during a major depressive episode and its relationship with other clinical variables, such as the lifetime history of suicide attempts. Study IV. Another post-hoc analysis of the BRIDGE-II-Mix study focused on the clinical relevance of the intertwined association between affective lability and mood reactivity and their correlation with other mixed symptoms, particularly verbal or physical hetero-aggression and suicide attempts. Study V. A critical systematic review of guidelines on the treatment of mixed states with a methodological quantitative quality assessment of included articles and a specific focus on challenging aspects such as hetero- and self-aggression. One every fourteen patients suffering from bipolar disorder reported violent criminal behavior. Even though the association with violent criminality was not significant when patients suffering from bipolar disorder were compared with patients suffering from any other psychiatric disorder, the chance of committing violent criminal behavior was smaller in patients with bipolar disorder than in those suffering from psychotic disorders but higher in comparison with patients with depressive disorders. In meta-regression analyses, no significant moderators emerged. The associations for violent criminal behaviors in bipolar disorder in comparison with patients suffering from anxiety, alcohol and drug abuse/dependence and personality disorders were not significant. Mood disorders as well as psychoses, borderline personality disorder and poly-drug use were the most relevant clinical predictors of deliberate self-harm in prison. In the sample of affective patients evaluated during a major depressive episode, the presence of aggressive behaviors was mainly related with bipolarity and the most relevant clinical variable associated with aggression was the presence of mixed features. A significant increase of the risk for aggressive behaviors associated with the presence of lifetime suicide attempts has been observed. As for the association between affective lability with other mixed symptoms, irritable mood and impulsivity were directly significantly associated with affective lability. These two clinical features are two of the most important mediators of self-aggressive behaviors. Despite this, affective lability was not correlated with a higher rate of suicide attempts.
The identification of self- and hetero-aggressive behaviors represented the target of a tailored treatment strategy in the subgroup of bipolar disorder patients characterized by a shared psychopathological “aggressive” dimension and mixed characteristics. in conclusion, the self- and hetero-aggressive components of bipolar disorder have been investigated in this doctoral thesis, leading to a better and broader knowledge on the topic, with important implications for the every-day clinical practice and in terms of treatment strategies, both in psychiatric and in correctional settings.El objetivo principal de esta tesis doctoral fue evaluar los correlatos clínicos de auto o hetero-agresiones, en el contexto del trastorno bipolar, con especial foco en aquellos pacientes que presentan características clínicas mixtas. Los cinco artículos incluidos tenían diseños de estudio diferentes: I. Meta-análisis de estudios sobre la asociación entre trastorno bipolar y conductas criminales violentas; II. Estudio transversal que evalúa los correlatos clínicos de autolesiones e intentos de suicidio en presos, en particular trastornos afectivos y trastorno bipolar; III. Análisis post-hoc del estudio BRIDGE-II-MIX, con el objetivo de evaluar la hetero-agresión considerada como característica mixta durante un episodio depresivo, y su relación con otras variables clínicas, como la historia de intentos de suicidio; IV. Análisis post-hoc del estudio de BRIDGE-II-MIX, enfocado en la importancia clínica de la asociación entrelazada entre la labilidad afectiva y la reactividad de humor y su correlación con otros síntomas mixtos, en particular la hetero-agresión verbal o física; V. Revisión crítica sistemática de guías clínicas sobre el tratamiento de estados mixtos con una evaluación cuantitativa de la calidad metodológica de los artículos incluidos. Uno cada catorce pacientes que padecen de trastorno bipolar presentó una conducta criminal violenta. La posibilidad de cometer una conducta criminal violenta era menor en pacientes con trastorno bipolar que en aquellos que padecen de trastornos psicóticos, pero mayor en comparación con pacientes con trastornos depresivos. Los análisis de meta-regresión no detectaron moderadores significativos. Los trastornos afectivos así como las psicosis, el trastorno límite de personalidad y el consumo de diferentes tóxicos eran los factores clínicos de riesgo más relevantes de autolesiones en la cárcel. En la muestra de pacientes afectivos evaluados durante un episodio depresivo, la presencia de comportamientos agresivos principalmente fue relacionada con la bipolaridad y la variable más relevante clínica asociada con agresión, fue la presencia de características mixtas. Se observó además un aumento significativo del riesgo para comportamientos agresivos asociados con la presencia de intentos suicidas previos. La identificación de comportamientos auto y hetero-agresivos representa el objetivo de una estrategia de tratamiento adaptada en el subgrupo de pacientes con trastorno bipolar, caracterizado por una dimensión psicopatológica "agresiva" compartida.
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Päären, Aivar. "Long-Term Health Outcome of Adolescent Mood Disorders : Focus on Bipolar Disorder." Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-239835.
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There has recently been an intense debate about the increased rate of bipolar disorders (BPD) in children and adolescents observed in clinical settings. Thus, there is great interest in child and adolescent symptoms of hypomania and whether these symptoms subsequently will develop into BPD. More knowledge about early signs could give insight into the development of the disorder. There are also concerns that hypomanic symptoms in adolescence indicate excess risk of other health conditions. It has been reported that patients with mood disorders have a high consumption of prescription drugs in different ATC classes. The primary objective of this thesis was to better understand the mental health outcome of adolescents with hypomania spectrum symptoms and to identify early risk factors for adult bipolar disorder among adolescents with mood disorders. In order to widen the scope and investigate health outcome of mood disorder in general psychopharmacological outcomes were included. A community sample of adolescents (N=2 300) in the town of Uppsala, Sweden, was screened for depressive symptoms. Both participants with positive screening and matched controls (in total 631) were diagnostically interviewed. Ninety participants reported hypomania spectrum episodes, while another 197 fulfilled the criteria for major depressive disorder (MDD) without a history of a hypomania spectrum episode. A follow-up after 15 years included a blinded diagnostic interview, a self-assessment of personality disorders, and national register data on prescription drugs and health services use. Adolescent mood symptoms, non-mood disorders, and family characteristics were assessed. Univariate and multivariate analyses were used. The results indicate that the phenomenology of the hypomania spectrum episodes during childhood and adolescence per se does not predict adult bipolar disorder. However, having both affective symptoms during adolescence and a family history of bipolar disorder increases the risk of developing bipolar disorders in adulthood. Disruptive disorder in childhood or adolescence as well as family histories of BPD emerged as significant risk factors that differentiated between the future development of BPD and MDD. Adolescents with hypomania spectrum episodes and adolescents with MDD do not differ substantially in health outcomes in adulthood. Both groups are at increased risk for subsequent mental health problems, high consumption of prescription drugs, and high health care use, compared with the control group. The high rates of prescription drugs in many ATC classes found among the former depressed females seem to indicate a series of co-morbid somatic illnesses. Thus, it is important to identify and treat children and adolescents with mood disorders, and carefully follow the continuing course. Characteristics such as disruptive disorders and family history warrant particular attention.
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Alamian, Golnoush. "Intellectual functioning in first-episode schizophrenia, schizoaffective disorder and bipolar disorder." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/51790.
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Intellectual functioning (IQ) prior to the onset of illness (premorbid IQ) and the pattern of its trajectory across illness onset can inform us of the early developmental pathology of mental disorders. The goals of this study were to 1) investigate these features in first-episode psychiatric patients with overlapping symptoms including schizophrenia (SZ), schizoaffective disorder (SA) and bipolar disorder (BD), as well as to 2) examine these features and the presence of psychosis, and the influence of mood-incongruent features, in BD patients. To address these objectives, SZ, SA, BD-I, and healthy controls, aged 17-37 years, were pooled from two early-intervention programs. The North American Adult Reading Test was used to estimate premorbid IQ, while the Kaufman Brief Intelligence Test was used to measure current IQ. Group differences in premorbid IQ and IQ trajectories were evaluated with ANOVA and repeated measure ANOVA. Both controls and BD patients had significantly higher premorbid IQ compared to SZ patients, BD patients had scores comparable to control, and there was a strong trend of premorbid IQ deficit in SA patients. Regarding IQ change, only subjects with SA and SZ experienced significant IQ deterioration through illness onset. Regarding psychosis, t-tests deciphered a strong, although insignificant, premorbid IQ difference across BD patients, with deficits seen in psychotic but not non-psychotic patients. Lastly, t-tests revealed a significant decline in IQ across psychotic BD patients with mood-congruent, and not –incongruent, features. Secondary post-hoc analyses revealed that this finding might be attributable to the type of antipsychotic that patients received. Taken together, these results suggest that early neurodevelopmental pathology, which most likely directly affects intellectual functioning, may be different in BD than in SA and SZ. Furthermore, low premorbid IQ could be a potential risk factor for psychosis. Assessment of IQ before and after illness onset could help facilitate early identification of psychopathology and assist with patient management and care.Medicine, Faculty of
Graduate
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Holt, Jim. "Biopolar Disorder." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/6500.
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Hale, Sandra. "Employment experiences of people with bipolar disorder." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/38196.
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The mental illness called bipolar disorder creates enormous social, economic and health implications for Canadian society. Bipolar disorder (BD) causes fluctuating mood states ranging from depression to mania. Over half a million Canadians live with BD (Schaffer, 2006), and approximately 400,000 are working age, 25-64 years (Wilkins, 2004). In Canada, reported prevalence of unemployment for all persons living with a severe mental illness, including BD, is as high as 90% (Kirby, 2006). The aim of this study was to explore the perspectives of people living with bipolar disorder regarding their employment accomplishments and obstacles, and to understand the adaptive strategies they used to manage both BD and employment. Using a qualitative research framework based primarily on the interpretive descriptive approach, considered especially suited to inform health care practice, purposive sampling identified 10 people living with the extreme mood fluctuations of BD type I. Their experiences were described during one in-depth interview, a follow-up telephone interview, and findings verified through written feedback. Three main themes were revealed, related to (1) hypomania and mania, (2) stigma and disclosure, and (3) employment factors that supported or created obstacles to successful employment. Findings suggest a broader perspective of employment issues should be considered by practitioners and employers to help reduce limitations encountered by this sample of persons with BD type I. Inclusion of social, psychoeducational and organizational issues in the repertoire of job accommodations may improve employment for this population.
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Woollatt, Julia. "An exploration of stigma in bipolar disorder." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531947.
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Sambrook, Suzanne. "A cognitive investigation of bipolar affective disorder." Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242667.
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Palmier-Claus, Jasper. "Childhood adversity in bipolar disorder and psychosis." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/childhood-adversity-in-bipolar-disorder-and-psychosis(40707dae-c064-4da5-8b06-2d7f18ff5b14).html.
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Study one is a meta-analysis of the relationship between childhood adversity and bipolar disorder. The results suggest that individuals with bipolar disorder are 2.63 times more likely to experience childhood adversity than non-clinical controls. This effect remained significant even when controlling for bias and when considering epidemiological and case control studies separately. Levels of adversity in bipolar disorder were comparable to those observed in samples diagnosed with unipolar depression and schizophrenia. In adversity subtype analysis, emotional abuse conveyed the greatest risk of bipolar disorder with an odds ratio of 4.04. The results suggest that childhood adversity, particularly emotional abuse, may play an important role in the development of bipolar disorder. This challenges the notion that bipolar disorder is solely the result of a genetic predisposition. Study two is cross-sectional research investigating the association between childhood adversity and social functioning across the continuum of psychosis, and possible mediators of this relationship (i.e. attachment style, theory of mind ability, clinical symptoms). Fifty-four clinical and 120 non-clinical participants completed self-report questionnaires, interviews and tasks of theory of mind ability. The author used multiple group structural equation modelling to fit mediation models, whilst allowing for differential relationships across the samples. In the final model, only depression mediated the relationship between childhood adversity and social functioning. Childhood adversity did not significantly predict theory of mind ability in this data. The results suggest that psychosocial interventions for improving social functioning should also target low mood, particularly in individuals with a history of childhood adversity. Taken together this thesis suggests that childhood adversity can have long-reaching and negative effects on individuals' mental well-being. The author explores the wider clinical, academic and theoretical implications, and potential limitations, of the research in paper three. This section also contains the author's reflections on the research process and a justification of key methodological and analytical decisions.
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Di, Florio Arianna. "Bipolar disorder in pregnancy and the postpartum." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/45405/.
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In the first part of my PhD I explored the link between childbirth and mood disorders in a retrospective sample of over 1500 parous women with mood disorders, recruited as part of ongoing molecular generic studies. Around two thirds of participants reported at least one episode of illness during pregnancy or the postpartum. Women with bipolar I disorder reported an approximately 50% risk of a perinatal major affective episode. Risks were lower in recurrent major depression and bipolar II disorder at around 40%. The majority of perinatal episodes occurred within 4 weeks of childbirth. Episodes of mania or psychosis had an earlier onset than those of depression. For bipolar II disorder, onsets of psychiatric episodes were more spread out over the perinatal period with more onsets in pregnancy and later in the postpartum. Moreover, childbirth did not seem to be a specific trigger for the majority of perinatal episodes of bipolar II disorder. Primiparity was associated with postpartum mania/psychosis and unipolar postpartum depression in women who experienced their first lifetime episode within 6 weeks postpartum. My findings raise the possibility of a relationship between postpartum mood disorders and other disorders influenced by parity, such as pre-eclampsia. In the second part of my PhD I designed and piloted a prospective study aimed i) to replicate and ii) to extend the findings on the retrospective sample, exploring the influence of a range of variables on the vulnerability to develop an episode of severe illness in pregnancy or the postpartum. Over 14 months of recruitment 19 women completed the follow-up assessment. To capture the clinical complexity of bipolar disorder in pregnancy and the postpartum period very large scale longitudinal studies are needed. These studies must be based on a strong collaboration with the NHS.
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Mezes, Barbara. "Understanding personal recovery experiences in bipolar disorder." Thesis, Lancaster University, 2018. http://eprints.lancs.ac.uk/127297/.
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Getz, Glen Edward. "FACIAL AFFECT RECOGNITON DEFICITS IN BIPOLAR DISORDER." University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin985628344.
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Wood, Christy Jean. "A Resource: Spiritual Companionship and Bipolar Disorder." Ashland Theological Seminary / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=atssem1573490368840156.
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Gregory, J. "Intrusive memories and images in bipolar disorder." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1443980/.
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The clinical literature on the phenomenology of intrusive memories and intrusive images was reviewed systematically. The methodology adopted in the literature is described before presenting the phenomenological findings of intrusive memories and intrusive images across the following categories: 1) prevalence, 2) sensory qualities, 3) emotions and 4) characteristics. The similarities and differences between intrusive memories and intrusive images across clinical disorders are discussed. It is then considered whether intrusive memories and intrusive images represent separate phenomenon and a pragmatic model is briefly presented to conceptualise the distinctions that may exist. Finally, areas of further research are presented.
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Jenkins, Melissa M. Youngstrom Eric Arden. "Clinical decision-making and pediatric bipolar disorder." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2745.
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Thesis (M.A.)--University of North Carolina at Chapel Hill, 2009.Title from electronic title page (viewed Mar. 10, 2010). "... in partial fulfillment of the requirements for the degree of Master of Arts in the Department of Psychology Clinical Psychology." Discipline: Psychology; Department/School: Psychology.
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Bunch, Kristin. "Risk taking behaviour in bipolar affective disorder." Thesis, University of Leeds, 2010. http://etheses.whiterose.ac.uk/1176/.
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This piece of research was designed to explore the nature of risk taking behaviour and impulsivity in bipolar affective disorder. Involvement in pleasurable activities that have a high potential, or risk, for unwanted consequences forms one of the DSM IV diagnostic criteria for (hypo)mania; however, little research has investigated the prevalence of risk taking behaviour in this population, nor the possible meaning of such behaviour. Furthermore, research has demonstrated that individuals diagnosed with bipolar disorder have elevated trait levels of impulsivity, as well as increased levels of state impulsivity during mood episodes. Much research has theoretically linked impulsivity with risk taking behaviour; however, little research has measured both constructs simultaneously. Therefore, this research was designed to measure both the propensity to engage in risk taking behaviour and levels of impulsivity via multiple methods in individuals diagnosed with bipolar disorder who were currently euthymic, to establish a baseline measure in the absence of clinically significant symptomatology. Two control groups were used; one was comprised of individuals with no history of psychiatric disorder and a group of individuals diagnosed with major depressive disorder, to establish the specificity of any findings to bipolar disorder rather than affective disorders in general. The bipolar group scored more highly on the behavioural measure of impulsivity and some aspects of the self-report measure than the two control groups, who did not differ significantly. the two clinical groups also reported higher levels of unhelpful coping strategies when experiencing depressed mood, including engaging in dangerous activities; however, there were no between groups differences on the behavioural risk taking task. The findings were discussed in relation to psychological models of bipolar disorders. Limitations of the research and ideas for future research were also discussed.
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Blowers, Helena. "Physical activity and mood in bipolar disorder." Thesis, University of Exeter, 2016. http://hdl.handle.net/10871/23111.
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Systematic review Background: Bipolar disorder is associated with a higher rate of physical health problems and lower levels of physical activity than other clinical and general populations. Despite the potential benefits of physical activity to people with bipolar disorder, little research has been published around this and no recent review of this topic is available. Due to the clinical utility of summarising the available research evidence on this topic, this review aimed to answer the question “Is physical activity associated with manic and depressive symptoms in people with bipolar disorder?”. Methods: Seven electronic databases were searched using a range of search terms to reflect physical activity and bipolar disorder variables. Results: Ten studies were identified that reported associations between physical activity and mood symptoms of bipolar disorder. There were inconsistent findings on the relationship between physical activity and mood, in particular with relation to manic symptoms, with reports of physical activity being both helpful and harmful to manic symptoms. Findings were more consistent with regards to the association between physical activity and depressive symptoms, with most showing that higher levels of physical activity are associated with lower depressive symptoms. Limitations: Many studies had small sample sizes and very few manipulated physical activity and included a control group. Measures and diagnosis method were heterogeneous. Four studies lacked a direct measure of manic symptoms. Conclusions: Results showed inconsistent findings with regards to the relationship between physical activity and mood symptoms and further research is needed to inform any guidelines developed for this client group. Empirical paper: Background: Despite the published evidence for the benefits of physical activity on mood in the general population and in people with mental illness, there is a lack of research into the associations between physical activity and mood in people with bipolar disorder. The current study therefore aimed to investigate the relationship between symptoms of mania and depression and different intensities, regularity, and total duration of physical activity per day and across the week. Methods: People with a diagnosis of bipolar disorder (N = 29) completed daily diaries on physical activity and manic and depressive symptoms over 14 days. Analysis included multilevel modelling, t-tests and correlation analysis. Results: No association was found between manic symptoms and physical activity, either at the within- or the between-person level. An association was found at the within-person level between higher duration of physical activity and lower depression symptoms, however no association was found at the between-person level. Limitations: The small sample size was adequate only to detect large-sized effects for between-person hypotheses. Participants were highly active and may not be representative of the wider BD population. Physical activity levels were assessed via self-report. Conclusions: The relationship between physical activity and manic symptoms in BD remains inconclusive, but a significant within-person association indicates that physical activity may reduce depressive symptoms in the short term. Given previous research on physical activity and manic symptoms, people with BD and professionals working with them may need to remain cautious, modifying any PA engagement depending on mood state.
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Walker, Megan Anna Hein. "bipolar[i].discuss()." Thesis, Virginia Tech, 2013. http://hdl.handle.net/10919/23805.
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This MFA thesis uses the medium of computer language to explore the chaos underlying Bipolar I Disorder, an enigmatic and disruptive illness. Using creative coding to generate a series of abstract systems representing human traits, I explore the common truth that pervades the seemingly randomness of mental illness: we all break the same.Master of Fine Arts
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Edsall, Lee. "The impact of genetic variations in bipolar disorder /." Link to online version, 2006. https://ritdml.rit.edu/dspace/handle/1850/1878.
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Fulford, Daniel. "Goal-Striving and Affect in Bipolar I Disorder." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_theses/128.
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Although most research on bipolar I disorder has focused on biological models, recent investigation has elucidated the importance of psychosocial predictors of the course of illness. Theories of the Behavioral Activation System?s role in affect have helped unify biological and environmental explanations of the disorder. Along these lines, researchers have proposed that goal striving and attainment predict manic symptoms. In the current study, experience-sampling methodology was used to assess the relationship between fluctuations in goal striving and affect among 12 persons with bipolar I disorder and 12 without a history of mood disorder (control group). Participants completed measures of goal striving and affect three times each day for a period of three weeks. It was hypothesized that moving more quickly than expected toward a given goal would result in decreased subsequent effort toward that goal (coasting) for the control group, and increased subsequent effort (anti-coasting) for those with bipolar I disorder, with positive affect mediating the relationship in both cases. Results indicated that those in the bipolar I disorder group were significantly more likely to anti-coast than those in the control group. This finding, however, was explained primarily by gender, as men in the bipolar I disorder group showed no evidence of anti-coasting. In addition, there was no evidence of the mediating role of positive affect in these phenomena. Implications of the findings, limitations, and future directions are discussed.
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McIntosh, Andrew M. "Commonalities and differences between schizophrenia and bipolar disorder." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/24947.
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Schizophrenia and bipolar disorder share many symptoms but are difficult to separate on the basis of treatment response or prognosis. This had led to question their validity as disease entities. The evidence concerning their validity is introduced in chapter 1 of this thesis and chapter 2 discusses the evidence for structural and neuropsychology abnormalities in both disorders, and specifically whether these form a basis by which they can be separated. Particular attention is given to magnetic resonance imaging (MRI) studies in affected individuals and in unaffected family members. Chapter 3 is a systematic review and meta-analysis of structural MRI studies of bipolar disorder, comparing affected patients with both healthy controls and with schizophrenic subjects. Some evidence is found for regions which may separate patients with bipolar disorder from controls and from patients with schizophrenia. Chapter 4 outlines the methods for the main neuropsychological and MRI study of families affected by schizophrenia, bipolar disorder or both. The clinical and neuropsychological results are given in chapter 4 and the MRI results in chapter 5. This study finds some evidence that certain neuropsychological impairments are specific to a family history of schizophrenia. Certain reductions in grey matter, particularly in prefrontal areas, appear to be relatively specific to a genetic liability for schizophrenia. Other regions, particularly the anterior thalamus, may be affected in all patients and relatives. Furthermore these grey matter findings are associated with complementary white matter density reductions. Chapter 6 discusses some of the outstanding issues in terms of the separation of schizophrenia and bipolar disorder, and discusses the future of neuropsychological and brain imaging research in this area.
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Alsaif, Murtada. "Central and peripheral proteomic characterisation of bipolar disorder." Thesis, University of Cambridge, 2013. https://www.repository.cam.ac.uk/handle/1810/252286.
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Knott, Sarah. "Investigating susceptibility to bipolar disorder, migraine and epilepsy." Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/108607/.
Full textAbstract:
Epidemiological and clinical studies demonstrate a high degree of comorbidity between bipolar disorder (BD) and migraine. A relationship between BD and epilepsy is also suggested, with both disorders displaying phenotypically similar symptom profiles. The overall aim of this thesis was to further explore the relationship between BD and the neurological conditions of migraine, and epilepsy, within a large, well-characterised sample of individuals with BD. Data were utilised from the Bipolar Disorder Research Network (BDRN); a large (n > 6000) UK sample of individuals with a diagnosis of BD. Lifetime history of migraine and epilepsy were assessed within BDRN using questionnaire and telephone interview methods. Migraine was highly prevalent within the bipolar sample and was found to disproportionately affect those with bipolar II disorder. Bipolar subjects with comorbid migraine experienced a relatively distinct illness profile, with a multivariate model revealing migraine comorbidity to be characterised by an increased risk of suicide attempt and anxiety disorder. Further analysis of the migraine phenotype revealed that observed differences in the clinical presentation of BD associated with migraine were largely associated with the migraine with aura subtype. A high rate of self-reported epilepsy was identified within the bipolar sample and group differences were revealed in the clinical course of the bipolar illness according to the presence of self-reported epilepsy. Multivariate analysis revealed an independent association of a history of suicide attempt with self-reported epilepsy within BD. Findings from this thesis highlight the importance of identifying migraine and epilepsy within BD, and that their recognition and treatment may have a beneficial impact on the course of illness and outcome in BD. This thesis also suggests that these comorbidities may represent a clinically useful subgroup characterised by specific clinical features, and may provide an opportunity for subcategorising for future aetiological studies, potentially facilitating the identification of shared pathophysiological mechanisms.
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Malhi, Gurjhinder Singh Psychiatry Faculty of Medicine UNSW. "Functional magnetic resonance imaging studies in bipolar disorder." Awarded by:University of New South Wales. Psychiatry, 2005. http://handle.unsw.edu.au/1959.4/23299.
Full textAbstract:
Aim To determine the neural correlates of Bipolar Disorder (BD) using functional Magnetic Resonance Imaging (fMRI) in different phases of the illness. Methods Five fMRI studies were conducted in adult female BD patients and healthy matched comparison subjects. The first two studies examined patients with bipolar depression and hypomania using captioned-pictures to characterize mood-state related patterns of activation. The subsequent three studies investigated BD euthymia using emotional words and faces to identify a potential trait-marker. Results During depression, bipolar patients demonstrated additional subcortical activation in the thalamus, amygdala, hypothalamus and medial globus pallidus. In hypomania, patients again had additional subcortical activation involving the caudate and the thalamus. In both studies patients had prefrontal cortex activation, but the pattern differed from that in healthy subjects. These studies suggested a pattern of mood-state related subcortical recruitment for emotional processing in BD. The next set of studies examined euthymic BD patients to partition trait and state-markers. The first study used implicit positive and negative word-associated affect and found diminished responses to positive and negative affective words as compared to healthy subjects in both cortical and subcortical brain regions, in particular the cingulate, thalamus and caudate. The second study used the emotional Stroop task to elicit implicit affective processing and euthymic patients had less cortical and subcortical activation in response to affect, in particular decreased left ventral prefrontal cortex (BA47) activation. The final study used explicit emotional processing of fear and disgust to examine affective responses, and showed that patients were generally less responsive to disgust, but had comparatively greater activations to fear. Conclusions BD patients have a likely deficit in the ventral prefrontal cortex that is evident in euthymia. Prefrontal cognitive appraisal of emotions is constrained in euthymic, depressed and hypomanic phases, reflected in subcortical changes that suggest additional processing. The likely cause for this is a functional prefrontal cortex deficit that results in compensatory changes in emotional processing systems. Treatment probably stabilizes these systems without normalizing them. Our studies demonstrate the benefits of examining BD in its different phases, and future studies should attempt to emulate this in medication-free patients.
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Mamdani, Firoza. "Genetic variation and lithium response in bipolar disorder." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82285.
Full textAbstract:
The importance of genes in the etiology of bipolar disorder (BD) has been substantiated through family, twin and adoption studies. The search for susceptibility genes, however, has proved to be an arduous task with disease complexity leading to the non-replication of published results. We have used lithium treatment response as a classification variable, thus providing a phenotypically more homogeneous sample to work with. With this sample we carried out pharmacogenetic studies to identify genes involved in the etiology of BD and/or in the response to Li. The phosphoinositide and cAMP pathway have been shown to be involved in Li's mode of action. Thus, a gene responsible for regulating inositol metabolism (prolyl endopeptidase, PREP) and three cAMP responsive element binding proteins (CREB1-3) were investigated. We have found an association indicating a possible role of CREB1 and 2 in the etiology of BD and Li response. Further studies in larger, independent samples and the analysis of additional markers should be undertaken to confirm these findings.