E-Book, Englisch, 106 Seiten
Penberthy Persistent Depressive Disorders
2019
ISBN: 978-1-61334-505-4
Verlag: Hogrefe Publishing
Format: EPUB
Kopierschutz: 6 - ePub Watermark
E-Book, Englisch, 106 Seiten
Reihe: Advances in Psychotherapy - Evidence-Based Practice
ISBN: 978-1-61334-505-4
Verlag: Hogrefe Publishing
Format: EPUB
Kopierschutz: 6 - ePub 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
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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 |25|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). 2.1.3 Serotonin The serotonin transporter gene is the most studied with respect to PDD because it has a polymorphism (a “short” vs. “long” allele) that appears to slow down the synthesis of the serotonin transporter (Jans, Riedel, Markus, & Blokland, 2007). This reduces the speed with which serotonin neurons can adapt to changes in their stimulation. This polymorphism may influence a person’s sensitivity to stress, thus increasing vulnerability to depression. This is a good example of the diathesis–stress model of disease. In this case, stress is a precipitating factor for depression in patients with genetic vulnerabilities. Stress interacts with a patient’s genetic makeup to influence risk for developing PDD. Research to support this can be found in birth cohort studies. Specifically, Caspi et al. (2003) conducted a prospective study with a cohort of patients born around the same time (same birth cohort). They found that in their cohort, having a MDD in the past year was best predicted by the combination of |26|having the short allele (polymorphism) of the serotonin transporter gene and having had multiple stressful life events in the past 5 years. Such interactive findings have been consistently reported, and the effects of multiple genes and psychosocial stress on depression are only starting to be explored. 2.1.4 Dopamine Dopamine is increasingly thought to play an important role in the pathophysiology of MDD. Perceived threats or stress trigger the amygdala to increase levels of dopamine in the prefrontal cortex and the ventral striatum. Inhibitory feedback creates a return to homeostasis, but stress can disrupt the feedback system by alerting striatal levels of brain-derived neurotrophic factor. This abnormal feedback in patients with depression may reduce striatal dopamine causing additional anhedonia or other depressive symptoms such as the tendency to attribute inappropriate salience to even mildly negative stimuli (McClung & Nestler, 2008). In fact, a polymorphism in the dopamine type 2 receptor gene has been found to influence the effect of past stressful life events on current depressive mood (Elovainio et al., 2007). Again, we see a diathesis–stress model in action, with the dopamine system potentially influencing vulnerability to MDD via interaction with stress in the current environment of the individual. 2.1.5 Brain-Derived Neurotrophic Factor Another polymorphism that may moderate the interactive effect of the serotonin transporter and stress is located on the gene that codes for brain-derived neurotrophic factor. This is a growth factor that has an important role in the genesis, development, and survival of brain cells. A common polymorphism in this gene (“Val” vs. “Met”) affects intracellular transport and secretion of brain-derived neurotrophic factor, impacting the hippocampus size and functioning, leading to hippocampal hypersensitivity to stress (Bath & Lee, 2006) and ultimately depression. There also appears to be an additive effect of having the short allele of the serotonin transporter, the Met allele and psychosocial stress, with an increased risk of depression resulting from having all three, even if the stress took place in childhood. Further evidence for a role of brain-derived neurotrophic factor in the pathophysiology of MDD comes from postmortem studies, which have found low levels of brain-derived neurotrophic factor in the hippocampus and prefrontal cortex of symptomatic depressed patients (Martinowich, Manji, & Lu, 2007). 2.1.6 Neuroendocrine Models In studies of the impact of psychosocial adversity during childhood on the risk of adult depression, it is often difficult to separate the effects of genes from those of the environment. This is because in the early environment, the same genetics are often at work in parents and children (e.g., when they are |27|biologically related), informing behaviors of both. Thus, studies with nonhumans are used to help us understand the interaction of genes and stress. For example, monkeys temporarily reared by peers rather than by their mothers develop exaggerated stress responses associated with abnormalities in serotonin activity as well as in the...
