E-Book, Englisch, 106 Seiten
Penberthy Persistent Depressive Disorders
2019
ISBN: 978-1-61676-505-7
Verlag: Hogrefe Publishing
Format: PDF
Kopierschutz: 1 - PDF Watermark
E-Book, Englisch, 106 Seiten
Reihe: Advances in Psychotherapy - Evidence-Based Practice
ISBN: 978-1-61676-505-7
Verlag: Hogrefe Publishing
Format: PDF
Kopierschutz: 1 - PDF Watermark
This compact guide is packed with the latest knowledge on the assessment and treatment of persistent depressive disorders (PDDs)
– the new DSM-5 diagnosis that amalgamates the categories dysthymic disorder (DD), chronic major depression (MDD), and DD with
major depressive episode (MDE).
Written by a leading expert, the book guides us through the complexities of assessing PDDs and the models for understanding how
these difficult-to-identify and potentially life-threatening disorders develop and are maintained over long periods. It then outlines
those therapies that have the strongest evidence base. The author goes on to explore in detail the cognitive behavioral analysis system
of psychotherapy (CBASP), a treatment specifically developed for PDDs. This compelling integrated approach incorporates components
of learning, developmental, interpersonal, and cognitive theory with aspects of interpersonal mindfulness. We are led expertly
through the therapeutic process using clinical vignettes and practical tips, with particular attention paid to identifying the assessment
and therapy methods most valuable in CBASP. Printable tools in the appendices can be used in daily practice.
This book will interest clinical psychologists, psychotherapists, psychiatrists, counselors, and students.
Zielgruppe
Clinical psychologists, psychiatrists, psychotherapists, and counselors, as well as students.
Autoren/Hrsg.
Fachgebiete
Weitere Infos & Material
1;Persistent Depressive Disorders;1
1.1;Table of Contents;6
1.2;1 Description of Persistent Depressive Disorders;8
1.3;2 Theories and Models of Persistent Depressive Disorders;31
1.4;3 Diagnosis and Treatment Indications;44
1.5;4 Treatment;51
1.6;5 Further Reading;82
1.7;6 References;84
1.8;7 Appendix: Tools and Resources;99
2 Theories and Models of Persistent Depressive Disorders
The etiology of PDD can be conceptualized within a multifactorial biopsychosocial framework. The biopsychosocial model attributes disease outcome to the variable interactions of biological factors (genetic, biochemical, biological), psychological factors (mood, personality, behavior), and social factors (cultural, familial, socioeconomic). Accompanying this framework is a diathesis– stress model, which has been increasingly popular in describing the etiology of PDD. The diathesis–stress model explains a disorder as the result of an interaction between a predisposed vulnerability and current psychosocial stress. The influences within such a model include genetic and biological factors, developmental and learning history, social and cultural influences, coping strategies, personality, chronic stress, trauma, and medical illness. Although there are multiple theories and models used to explain the development and continuation of depression, less research has been conducted specifically for PDD. Current major theories or models of depression will be reviewed here, with a focus on PDD and models that have associated empirically supported treatment approaches for PDD.
2.1 Biological Models
All forms of PDD are thought to have strong biological components in their etiology. Depression has been associated with multiple neurochemical changes, including deficiencies in norepinephrine, serotonin, and dopamine, and to variations of dopamine autoreceptors, 5-GT receptors, alpha-NE or beta-NE receptors. These changes may also be influenced by hormonal variations that contribute to the vast array of individual differences biologically and symptom- wise within and across depressed patients. In addition, chronic stress or trauma can provoke, exacerbate, or help maintain MDD, DD, and PDD.
2.1.1 Genetics
It is fairly well established that there is a genetic component of depression and that depression runs in families (Howland & Thase, 1991). Prevalence rates of MDD, DD, and double depression differ in families, suggesting their distinctions, even though they have substantial similarities. Environmental stress may be a greater influence in the etiology of DD, less severe depression, or early-onset depression than in the etiology of MDD, and the genetic contribution appears to be greater for more severe, recurrent, melancholic, or psychotic depression (Griffiths, Ravindran, Merali, & Anisman, 2000).
Scientists have not found a specific gene or series of genes that cause depression, but have found certain variations in genes, called polymorphisms, that may increase the risk for depression. Genes and their variations are important because they help control the metabolism of neurotransmitters and their receptors, and they control the numbers of particular types of neurons and their synaptic connections, the intracellular transduction of neuronal signals, and the speed with which all of these can change in response to environmental stressors (Lohoff, 2010).
2.1.2 Monoamine Hypothesis
The monoaminergic systems (serotonin, norepinephrine, and dopamine) have received the most attention in the neurobiology of MDD, and most classes of antidepressants target these monoaminergic systems. Investigation into the neurobiology of depression has especially focused on serotonin and norepinephrine (Lohoff, 2010). An enzyme called monoamine oxidase is involved in removing serotonin and dopamine from the brain. The monoamine hypothesis posits that depressed patients have low levels of these neurotransmitters and that antidepressant medications that increase the levels help improve depressive symptoms. We know that unfortunately this does not happen for every patient. Additionally, research has demonstrated that lowering serotonin levels does not induce depression in all people (Cools et al., 2005). Overall, there appear to be several factors that contribute to a patient’s vulnerability to the effects of lowered serotonin on depressive symptoms. There is evidence for biological differences within chronically depressed patients, with strong support for a greater monoamine oxidase imbalance in early-onset DD versus late-onset DD (Versiani, Amrein, Stabl, & International Collaborative Study Group, 1997).
