E-Book, Englisch, 114 Seiten
Abramowitz / Jacoby Obsessive-Compulsive Disorder in Adults
1., 2015
ISBN: 978-1-61676-411-1
Verlag: Hogrefe Publishing
Format: PDF
Kopierschutz: 1 - PDF Watermark
E-Book, Englisch, 114 Seiten
Reihe: Advances in Psychotherapy - Evidence-Based Practice
ISBN: 978-1-61676-411-1
Verlag: Hogrefe Publishing
Format: PDF
Kopierschutz: 1 - PDF Watermark
Cognitive-behavioral therapy using the techniques of exposure and response prevention has helped countless individuals with obsessive-compulsive disorder (OCD) overcome debilitating symptoms and live fuller, more satisfying lives.
This volume opens with an overview of the diagnosis and assessment of OCD in adults and delineates an evidence-based conceptual framework for understanding the development, maintenance, and treatment of obsessions and compulsions.
The core of the book that follows is a highly practical treatment manual, based on decades of scientific research and clinical refinement, packed with helpful clinical pearls, therapist-patient dialogues, illustrative case vignettes, sample forms and handouts. State-of-the-art strategies for enhancing exposure therapy using inhibitory learning, ACT, and couples-based approaches are described. Readers are also equipped with skills for tailoring treatment
to patients with different types of OCD symptoms (e.g., contamination, unacceptable
thoughts, challenging presentations such as mental rituals) and for addressing common
obstacles to treatment. The book is an essential resource for anyone providing
services for individuals with anxiety disorders.
Autoren/Hrsg.
Fachgebiete
Weitere Infos & Material
1;Obsessive-CompulsiveDisorder in Adults;1
1.1;Table of Contents;8
2;1 Description;10
3;2 Theories and Models;21
4;3 Diagnosis and Treatment Indications;28
5;4 Treatment - 4.1 Methods of Treatment;37
6;4.2 Mechanisms of Action;79
7;4.3 Efficacy and Prognosis - 4.4 Variations and Combinations of Methods;80
8;4.5 Problems in Carrying Out the Treatment;82
9;4.6 Multicultural Issues;89
10;5 Case Vignettes;91
11;6 Further Reading;100
12;7 References;101
13;8 Appendix: Tools and Resources;103
2 Theories and Models (p. 12-13)
A number of theories have been proposed to explain the development and clinical picture of OCD. This chapter reviews several theoretical models that have been well-studied, with an emphasis on the cognitive-behavioral model which forms the basis of the treatment program described in Chapter 4.
2.1 Biological Theories
2.1.1 Neurotransmitter Theories
Biological models of OCD can be categorized into neurotransmitter and neuroanatomical theories. Prevailing neurotransmitter theories propose that abnormalities in the serotonin system, particularly the hypersensitivity of postsynaptic serotonergic receptors, underlie OCD symptoms. This “serotonin hypothesis” was proposed following observations that serotonergic medication, but not other kinds of antidepressants, were effective in reducing OCD symptoms. However, results from numerous studies that have directly examined the relationship between serotonin and OCD have been inconsistent. For instance, some studies report increased concentrations of serotonin metabolites in the cerebrospinal fluid of OCD patients relative to nonpatients; other studies do not report such findings. Whereas the preferential response of OCD to serotonergic medication is often championed as supporting the serotonin hypothesis, this argument is of little value since the hypothesis was derived from this treatment outcome result. To date there are few convincing data to suggest that problems with serotonin functioning (or other neurotransmitters) mediate OCD symptoms.
2.1.2 Neuroanatomical Theories
Predominant neuroanatomical models of OCD propose that obsessions and compulsions arise from structural and functional abnormalities in particular areas of the brain, specifically the orbitofrontal-subcortical circuits. These circuits are thought to connect regions of the brain involved in processing information with those involved in the initiation of certain behavioral responses; and their over activity is thought to lead to OCD. Neuroanatomic models have been derived from imaging studies in which activity levels in specific parts example, positron emission tomography (PET) studies have consistently found increased glucose utilization in the orbitofrontal cortex (OFC) among patients with OCD as compared to nonpatients.
Although thought-provoking, neuroanatomical studies are cross-sectional and correlational, and therefore cannot address hypotheses about cause, such as whether OCD arises from apparent dysfunctions in the brain, or whether the observed alterations in brain function represent normally functioning brain systems that are simply affected by the presence of chronic obsessional anxiety; thus, the direction of causality remains unclear. Moreover, to date there is no biological (i.e., neurochemical, neuroanatomical, or genetic) test for OCD.
2.2 Psychological Theories
2.2.1 Learning Theory
Early learning (conditioning) models of OCD were drawn from Mowrer’s (1960) two-factor theory which proposes that pathological fear is acquired by classical conditioning and maintained by operant conditioning. For example, an obsessional fear of cemeteries is thought to arise from a traumatic experience during which anxiety becomes associated with such places. This fear is then maintained by behaviors that prevent the natural extinction of the fear, such as avoidance of cemeteries and funeral homes, and compulsive praying. Avoidance and rituals are negatively reinforced by the immediate (albeit temporary) reduction in discomfort that they engender. Thus, such behaviors develop into strong habits.
Research supports some aspects of the learning theory, but not others. For example, obsessional stimuli indeed evoke anxiety, and compulsive rituals do bring about an immediate reduction in anxiety and distress. However, traumatic conditioning experiences do not appear to be necessary for the development of obsessions. Contemporary cognitive-behavioral models (as described in Section 2.2.3) were subsequently formulated to explain the development of obsessional fear.
2.2.2 Cognitive Deficit Models
Because people with OCD sometimes demonstrate the appearance of reduced performance on cognitive tasks such as executive functioning, cognitive inhibition, and some forms of memory, some theorists have proposed that OCD is characterized by deficits in neuropsychological and information-processing functioning. However, such impairment, if present at all, tends to be mild and of trivial clinical importance (Abramovitch, Abramowitz, & Mittleman, 2013). Moreover, these minor deficits could be caused by the effects of anxiety and fear which characterize OCD (as opposed to the other way around). Cognitive deficit models have two key limitations. First, they do not account for the heterogeneity of OCD symptoms (e.g., why some patients have contamination...
