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1
Balzafiore, Danielle, Thalia Robakis, Sarah Borish, Vena Budhan, and Natalie Rasgon. The treatment of bipolar disorder in women. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0020.
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Sex-specific effects in the clinical presentation and course of bipolar disorder in women have important treatment implications for the management of symptoms across the menstrual cycle and reproductive lifespan. Women with bipolar disorder are particularly vulnerable to premenstrual mood symptoms, menstrual abnormalities, and polycystic ovary syndrome. Special considerations include understanding the interactions between these reproductive issues, oral contraceptives, and mood-stabilizing agents. Additionally, the management of bipolar disorder during the perinatal period requires a careful approach to psychotropic medication to optimize the maintenance of mood stability while minimizing the potential for adverse risk of fetal and neonatal outcomes. Non-pharmaceutical approaches, including electroconvulsive therapy, transcranial magnetic stimulation, selected psychotherapies, and social and behavioural interventions may represent efficacious treatment options to reduce medication burden. Lastly, women with bipolar disorder may be at particular risk for worsening of affective symptoms during the menopausal transition, and strategies to reduce sleep disruption are imperative.
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Bipolar disorders: Clinical course and outcome. Washington, DC: American Psychiatric Press, 1999.
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(Editor), Joseph F. Goldberg, and Martin Harrow (Editor), eds. Bipolar Disorders: Clinical Course and Outcome (Clinical Practice). American Psychiatric Publishing, Inc., 1999.
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4
Youngstrom, Eric, and Anna Van Meter. Comorbidity of Bipolar Disorder and Depression. Edited by C. Steven Richards and Michael W. O'Hara. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199797004.013.003.
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There has been speculation about the relationship between depression and mania for centuries. Modern psychiatry and psychology have mostly viewed these as different subtypes within a “family” of mood disorders. Conceptual models of comorbidity provide an opportunity to re-examine the association between depression and other pathological mood states. We examine the evidence pertaining to rates of “comorbidity,” which, in this case, refer to the lifetime occurrence of depression and hypomanic, mixed, or manic episodes in the same individual. We explore factors that could contribute to artifactual comorbidity. We also examine data pertaining to similarities or differences in phenomenology, longitudinal course, associated features, family history, and treatment response. Multiple factors are likely involved in the comorbidity of depression and hypomania or mania, and the problems of poor reliability and inconsistent diagnostic definitions and methodology attenuate the significance of most research findings. However, evidence appears sufficient to conclude that not all depression is on the bipolar spectrum, that bipolar features moderate the course and outcome of depressive illness, and that depression and bipolar disorder most likely involve a blend of some shared and some specific mechanisms. Research and clinical work both will advance substantially by more systematically assessing for potential bipolar features “comorbid” with depression and following how these factors change the trajectory of depression over time.
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Henter, Ioline D., and Rodrigo Machado-Vieira. Novel therapeutic targets for bipolar disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0030.
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The long-term course of bipolar disorder (BD) comprises recurrent depressive episodes and persistent residual symptoms for which standard therapeutic options are scarce and often ineffective. Glutamate is the major excitatory neurotransmitter in the central nervous system, and glutamate and its cognate receptors have consistently been implicated in the pathophysiology of mood disorders and in the development of novel therapeutics for these disorders. Since the rapid and robust antidepressant effects of the N-methyl-D-aspartate (NMDA) antagonist ketamine were first observed in 2000, other NMDA receptor antagonists have been studied in major depressive disorder (MDD) and BD. This chapter reviews the clinical evidence supporting the use of novel glutamate receptor modulators for treating BD—particularly bipolar depression. We also discuss other promising, non-glutamatergic targets for potential rapid antidepressant effects in mood disorders, including the cholinergic system, the melatonergic system, the glucocorticoid system, the arachidonic acid (AA) cascade, and oxidative stress and bioenergetics.
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Fountoulakis, Konstantinos N., and Dimos Dimellis. The treatment of rapid cycling bipolar disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0006.
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Rapid cycling may complicate the course of a significant proportion of patients with bipolar disorder (BD). It is defined in DSM-5 by the occurrence of at least four distinct mood episodes in 12 months. Rapid cycling BD has been consistently associated with worse outcomes compared with non-rapid cycling BD. Thus, rapid cycling BD may require specific treatment strategies. Antidepressants, antipsychotics, and mood stabilizers/anticonvulsants have been studied either as monotherapy or in combination treatments. Concerning the treatment of acute mood episodes, the best available data exist for atypical antipsychotics. On the other hand, maintenance or relapse-prevention treatment, and newer-generation antipsychotics and anticonvulsants seem to be efficacious for rapid cycling BD. Lithium may also be efficacious. Treatment with antidepressants should be avoided in this subpopulation of patients. Overall, few randomized controlled trials have been conducted, and many have been underpowered. Therefore, a significant gap remains in evidence-based treatment of rapid cycling BD.
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Milev, Roumen. The role of electroconvulsive therapy in the treatment of bipolar disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0027.
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This chapter examines the use of electroconvulsive therapy (ECT) for treatment of patients with bipolar disorders. It briefly reviews the basics of ECT, stimulus parameters, placement of electrodes, and seizure threshold. The data for efficacy and tolerability of ECT for bipolar disorder, including mania, depression, mixed states, and across the lifespan is reviewed. Although there is a paucity of good-quality randomized studies, all available data, including case reports and naturalistic observations, support the use of ECT in this population, and reinforce the widespread use of ECT in everyday clinical practice. Good-quality randomized control trials are urgently needed to address numerous unanswered questions, in order to improve efficacy and reduce side-effect burden of one of the best treatments for bipolar disorder.
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Cavalcante Passos, Ives, and Flávio Kapczinski. Staging and neuroprogression in bipolar disorder: treatment implications. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0024.
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It is known that if, not all, a substantial proportion of patients with bipolar disorder (BD) present a progressive course with functional and cognitive impairment. In addition, patients with BD and multiple mood episodes have a worse response to lithium and cognitive behaviour therapy. However, many current treatment guidelines do not take these clinical features that change with illness progression into account. In order to clarify these clinical questions, the term ‘neuroprogression’ was conceptualized as the pathological rewiring of the brain that takes place in parallel with the clinical deterioration in the course of BD. It provides a heuristic basis for conceptualizing the biochemical foundation of changes in brain circuits related to the progressive course of BD. Herein, we aim to review risk factors, biological underpinnings, and treatment implications related to neuroprogression in BD.
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Fabbri, Chiara, and Alessandro Serretti. The treatment of bipolar disorder in the era of personalized medicine: myth or promise? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0031.
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Bipolar disorder (BD) is a chronic disease associated with high personal and socio-economic burden. Genetics accounts for 20–95% of variability in central nervous system drug disposition and pharmacodynamics, thus genetic markers are considered a promising way to develop tailored treatments and improve the prognosis of the disease. Among mood stabilizers, lithium response was the most investigated phenotype and the most replicated genes are involved in synaptic plasticity (BDNF), serotonergic (SLC6A4) and dopaminergic (DRD1) neurotransmission, and second messenger cascades (GSK3B). Relevant pharmacogenetic findings regarding other mood stabilizers are hyperammonaemia (CPS1 gene) and hepatic dysfunction (POLG gene) induced by valproate and immune-mediated cutaneous hypersensitivity reactions (HLA-B*1502) induced by lamotrigine or carbamazepine. Polymorphisms in cytochrome (CYP) P450 genes are expected to provide useful information particularly in case of polypharmacy. Despite few pharmacogenetic tests are currently recommended, the development of pharmacogenetics in other fields of medicine provides an encouraging perspective.
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da Costa, Sabrina C., Joao L. de Quevedo, and André F. Carvalho. Predominant polarity, polarity index, and treatment selection in bipolar disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0015.
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Bipolar disorder (BD) is a chronic and disabling illness, with lifetime prevalence of 2.4% worldwide. Predominant polarity (PP), ie, depressive versus manic, may influence illness characteristics, treatment selection, and outcomes in BD. PP has been proposed as a course specifier for BD, although not included in the Diagnostic and Statistical Manual of Mental Disorders (5th edn) (DSM-5). The polarity index (PI), a metric algorithm that reflects antimanic versus antidepressant maintenance efficacy of available treatments for BD, is calculated as the ratio of number needed to treat (NNT) for prevention of depression and NNT for prevention of mania. Evidence indicates that the net PI of ongoing maintenance-treatment regimens for BD is related to the patient’s PP. Additionatlly, PP and PI may aid in treatment selection and outcome prediction in BD. Therefore, this chapter provides an overview of putative roles of PP and PI in the course and treatment selection for BD.
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Frye, Mark A., Paul E. Croarkin, Marin Veldic, Malik M. Nassan, Katherine M. Moore, Simon Kung, Susannah J. Tye, William V. Bobo, and Jennifer L. Vande Voort. Evidence-based treatment of bipolar depression. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0007.
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Despite the predominant illness burden, evidence-based treatment, and by extension regulatory approved, for acute bipolar depression is significantly less than evidence bases in acute mania and maintenance treatment. Complicating this deficit has been persistent use of unimodal antidepressant therapy without clear and convincing benefit. Successful regulatory-approved drug development has focused on atypical antipsychotic therapy. Evidence-based treatments also include lamotrigine and divalproex by meta-analyses and a number of manual-based psychotherapies. In contrast, unimodal antidepressants as a class for bipolar depressed patients as a group appear to provide substantial benefit and may pose risk for mood destabilization. Promising novel and neuromodulatory treatments while encouraging require further systematic investigation. Understanding unimodal antidepressant response and risk patterns in bipolar disorder has immediate clinical implications. Moreover, evidence-based guidelines will need to bridge more individualized or precision-based treatment interventions.
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James, Anthony. Depressive Disorders in Childhood and Adolescence. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198801900.003.0008.
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This chapter focuses on depressive disorders in childhood and adolescence. Depression in children and adolescents is a complex and debilitating disease, and typically has a lifelong, chronic, and recurrent course. The peak age of onset of depression is between 13 and 15 years. After providing a clinical picture of depression, this chapter discusses early childhood depression and differential diagnosis, including paediatric bipolar disorder, psychotic depression and seasonal affective disorder, oppositional and conduct disorder, and substance misuse and medical conditions. It then examines comorbidity, paying attention to bipolar disorder and suicidal behaviour, along with the assessment and prevention of depression. It also considers some of the determinants of depression, such as stress, trauma, life events, and biological factors such as genetics, brain mechanisms, hormones, and resilience. Finally, it describes treatment options for childhood and adolescent depression.
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Meyer, Emma, Julie Walsh-Messinger, and Dolores Malaspina. Diagnosis and Epidemiology of Psychotic Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0012.
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Schizophrenia spectrum disorders and affective psychoses are jointly considered in this chapter in light of the ongoing controversy concerning the diagnostic boundary between these conditions. Emil Kraepelin first separated schizophrenia (which he named dementia praecox) from manic-depressive insanity based on the deteriorating course of illness in schizophrenia, and the convention is still upheld in the DSM-5. A wealth of evidence suggests that this dichotomy does not mirror clinical reality. This chapter reviews the history of the diagnostic concepts underlying the grouping and separation of “the psychoses,” focusing on schizophrenia, schizoaffective disorder, and bipolar disorder.
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Post, Robert M. Depression as a Recurrent, Progressive Illness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0003.
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Clinical Highlights and summary of Chapter• Episodes of depression and bipolar illness progress in two ways:faster recurrences as a function of number of prior episodes, andgreater autonomy (decreased need for precipitation by stressors(Episode Sensitization)• Recurrent stressors result in increased reactivity to subsequent stressors(Stress sensitization) and bouts of stimulant abuse increase in severity with repetition(Stimulant-induced behavioral sensitization)• Each type of sensitization cross-sensitizes to the others and drives illness progression• Each type of sensitization involves specific memory-like epigenetic processes as well as nonspecific cellular toxicities• Childhood onset depression and bipolar illness have a more adverse course than adult onset illness and are increasing in incidence via a cohort (year of birth) effect• As opposed to genetic vulnerability, each type of sensitization can be prevented with appropriate clinical intervention and prevention, which should lessen illness severity and progression• Seeing depression and bipolar disorder as progressive illnesses changes the therapeutic emphasis away from acute treatment and instead to long term prophylaxis• Preventing recurrent depressions will likely protect the brain, the body, and the personWord count with Named refs = 6,417>Depression and bipolar disorder are illnesses which tend to progress with each new recurrence. Stressors, mood episodes, and bouts of substance abuse each sensitize (show increased reactivity) upon their repetition and cross-sensitization to the others. These sensitization processes appear to have a memory-like and epigenetic basis, in some instances conveying lifelong increased vulnerability to illness recurrence and progression. Greater numbers of episodes are associated with faster recurrences, lesser need for stress precipitation, cognitive dysfunction, pathological changes in brain, treatment refractoriness, and loss of many years of life expectancy, predominantly from cardiovascular disease. Such a perspective emphasizes the need for greater awareness of higher incidence of psychiatric and medical comorbidities in the United States compared to many European countries, and the need for earlier intervention and more sustained long term prophylaxis to prevent illness progression and its adverse consequences on brain and body.
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Mueser, Kim T., Douglas L. Noordsy, and Robert E. Drake. Serious Mental Illness. Edited by Kenneth J. Sher. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199381708.013.009.
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The high comorbidity between substance use disorders and serious mental illnesses is a significant challenge to traditional treatment systems that have historically treated psychiatric and substance use disorders with different providers and agencies. Defining characteristics of serious mental illness include difficulty with work, performing in school or parenting, social difficulties, and problems caring for oneself. Common serious psychiatric disorders include schizophrenia, schizoaffective disorder, bipolar disorder, and severe major depression, posttraumatic stress disorder, and borderline personality disorder. The epidemiology of substance use disorders in serious mental illness is reviewed, including prevalence, correlates, and onset and course of the disorder. The clinical consequences of substance use disorders in this population are devastating for every possible aspect of the illness. Common factors may increase vulnerability to both substance abuse and psychiatric disorders. The principles of treating co-occurring disorders are based on modern integrated methods, as well as research on the effectiveness of integrated treatment.
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Lally, John, and James H. MacCabe. Epidemiology, impact, and predictors of treatment-resistant schizophrenia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198828761.003.0004.
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Treatment-resistant schizophrenia (TRS) is a disabling psychotic disorder that affects approximately 30% of those diagnosed with schizophrenia. In a significant proportion (about 70%) of patients with TRS, their illness is treatment-resistant from onset (early or primary treatment resistance), whilst, in the remainder, treatment resistance develops during the course of illness (late or secondary treatment resistance). TRS is associated with reduced quality of life and increased social and economic burden. Multiple sociodemographic, clinical, and biological risk factors have been assessed in relation to TRS, but their interpretation remains limited owing to methodological variation, lack of replicability, and a paucity of longitudinal studies. This chapter will review the epidemiology, societal and economic burden, and risk factors associated with TRS.
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Witkiewitz, Katie, and Connie Stauffer. Depression and Alcohol Use. Edited by C. Steven Richards and Michael W. O'Hara. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199797004.013.001.
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The World Health Organization (WHO) has identified alcohol and depression as the third and fourth largest risk factors for disease burden and leading causes of disability. Co-occurring alcohol-use disorder and depression has been linked to a more severe course of illness and worse treatment outcomes. In this chapter, we review the literature on alcohol use, depression, and their comorbidity. In addition to prevalence data we review common risk and protective factors that may impact comorbid alcohol-use disorder and depression, specifically focusing on individual differences and the environment including social and family factors, personality, cognitive, and other psychiatric factors, as well as genetic and neurobiological factors. Assessment and treatment approaches as well as clinical considerations for working with clients who have depression and co-occurring alcohol-use disorders are addressed.
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Richards, C. Steven, and Michael W. O'Hara, eds. The Oxford Handbook of Depression and Comorbidity. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199797004.001.0001.
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Depression is frequently associated with other psychiatric disorders, chronic health problems, and distressed close relationships. This comorbidity between depression and other disorders and problems is important. Furthermore, there has been a large increase in research on depressive comorbidity. Therefore, a book of 37 state-of-the-art reviews by experts will be helpful to teachers, researchers, practitioners, developers of relevant policies, and students in these areas. The comorbidity of depression with other psychiatric disorders is addressed in chapters focusing on panic disorder, post-traumatic stress disorder, social anxiety disorder, generalized anxiety disorder, alcohol-use disorders, eating disorders, conduct disorder, personality disorders, sexual dysfunctions, schizophrenia, suicide, and bipolar disorder. The comorbidity of depression and chronic health problems is addressed in chapters focusing on cardiovascular disease, cancer, pain, obesity, sleep disorders, multiple sclerosis, acquired immune deficiency syndrome, kidney disease, dementia, and women's health. The comorbidity of depression and distressed close relationships is addressed in chapters on intimate relationships, family relationships, and perinatal depression. There are also chapters on diagnostic issues, theory and constructs, models of comorbidity between depression and anxiety, assessment strategies, multidisciplinary treatments, community interventions, treatment in ethnic minority groups, psychosocial interventions for depressed cancer patients, and cognitive therapy for comorbid depression. Finally, in an effort to integrate the material, there are introduction, big picture, and epilogue chapters. The 37 chapters in this book reflect a scholarly and evidence-based perspective on depressive comorbidity. Moreover, the chapters address a wide array of relevant issues, including etiology, assessment, diagnosis, course, theory, research, practice, treatment, and clinical guidelines. In summary, this edited book includes 37 chapters on depression and comorbidity, and thereby provides a comprehensive, scholarly, and empirically-based compendium of reviews on this topic.
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Takeshita, Junko, and Joel M. Gelfand. Epidemiology of psoriasis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0002.
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Psoriasis is a common chronic inflammatory disorder of the skin that is associated with multisystem effects. Approximately 125 million people worldwide are affected by psoriasis, nearly one quarter of whom have moderate to severe disease. The majority of patients with psoriasis have a waxing and waning course with variable periods of spontaneous disease improvement or clearance. A rapidly expanding body of epidemiologic literature suggests psoriasis to be associated with a greater comorbid disease burden than patients without psoriasis. In addition to psoriatic arthritis, cardiometabolic diseases, including metabolic syndrome and its component disorders, as well as major adverse cardiovascular events are the most common comorbidities of psoriasis; together they are the primary cause of premature mortality among moderate to severe psoriasis patients. Continued efforts to better understand currently known and identify other emerging comorbidities of psoriasis are critical.