E-Book, Englisch, 94 Seiten
Spaulding / Silverstein / Menditto The Schizophrenia Spectrum
2. Auflage 2017
ISBN: 978-1-61676-504-0
Verlag: Hogrefe Publishing
Format: PDF
Kopierschutz: 1 - PDF Watermark
E-Book, Englisch, 94 Seiten
Reihe: Advances in Psychotherapy - Evidence-Based Practice
ISBN: 978-1-61676-504-0
Verlag: Hogrefe Publishing
Format: PDF
Kopierschutz: 1 - PDF Watermark
An essential reference for assessing and treating people with schizophrenia spectrum disorders – now updated and even more comprehensive.
The new edition of this highly acclaimed volume provides a fully updated and comprehensive account of the psychopathology, clinical assessment, and treatment of schizophrenia spectrum disorders. It emphasizes functional assessment and modern psychological treatment and rehabilitation methods, which continue to be under-used despite overwhelming evidence that they improve outcomes. The compact and easy-to-read text provides both experienced practitioners and students with an evidencebased guide incorporating the major developments of the last decade: the new diagnostic criteria of the DSM-5, introducing the schizophrenia spectrum and neurodevelopmental disorders, the further evolution of recovery as central to treatment and rehabilitation, advances in understanding the psychopathology of schizophrenia, and the proliferation of psychological and psychosocial modalities for treatment and rehabilitation.
Zielgruppe
Clinical psychologists, psychiatrists, psychotherapists, and
counselors, as well as students.
Autoren/Hrsg.
Fachgebiete
Weitere Infos & Material
1;Preface to the Second Edition and Contents;6
2;1 Description;10
3;2 Theories and Models of the Schizophrenia Spectrum;37
4;3 Diagnosis and Treatment Indications;50
5;4 Treatment;58
6;5 Case Vignettes;86
7;6 Further Reading;88
8;7 References;90
9;8 Appendix: Tools and Resources;100
2 Theories and Models of the Schizophrenia Spectrum (p. 28-29)
Modern etiological theories of the schizophrenia spectrum have two key features: (1) they make extensive use of the concept of vulnerability or diathesis- stress, and (2) they reflect a biosystemic paradigm in which biological, psychological, and social processes interact reciprocally. The second feature is the more recent development in the march of science. Many of the older theories have a reductionist connotation, i.e., they imply that “schizophrenia” can be reduced to specific genetic, neurophysiological, or neuroanatomical abnormalities. Such theories may still illuminate specific processes associated with neurodevelopmental psychopathology, but they need to be considered in a more holistic context. This section begins with a discussion of the key concept of vulnerability, and then, consistent with the biosystemic paradigm, turns to specific etiological mechanisms at biological, psychological, and social levels of functioning.
2.1 The Concept of Vulnerability
Decades before today’s consensus that schizophrenia is not a discrete, singular condition, it was clear that it had no single cause. On the one hand, genealogical research has long indicated involvement of heredity. Having a parent diagnosed with schizophrenia raises a child’s statistical risk from the general population rate of from about 1% or less to about 10%, even if the child is never in the care of the diagnosed parent. Having an identical twin with schizophrenia increases the risk to about 50%, even when the twins are raised separately. On the other hand, of people diagnosed, only a minority have any first-degree relatives with schizophrenia. To explain this paradox, Paul Meehl, a founding figure in clinical psychology, made a distinction between schizotaxia, schizotypy, and schizophrenia. Schizotaxia is the genetic component, and schizotypy is the hypothetical phenotype of schizotaxia that creates a vulnerability to actual schizophrenia. Schizotypy is a psychological construct, hypothesized to have trait-like properties, measurable by instruments like the Minnesota Multiphasic Personality Inventory (MMPI) and numerous self-report scales developed specifically for that purpose. Only a minority of people (about 10%) with schizotaxia and schizotypy are expected to actually develop schizophrenia, suggesting that the genetic vulnerability must interact with something else, perhaps environmental, to produce the disorder.
In the mid-1970s Joseph Zubin, another seminal figure in clinical psychology, and his student Bonnie Spring proposed that vulnerability is fundamental to understanding the etiology of schizophrenia. Diathesis, an older medical term similar in meaning to vulnerability, began to reappear in the literature, and the leading theory of schizophrenia became known as the diathesis-stress model. There was a major shift in psychopathology research, a new focus on abnormalities not only in people diagnosed with schizophrenia but also their biological relatives, and in children thought to be at risk, mostly because their parent had been diagnosed.
A focus on vulnerabilities was seen as antithetical to the neo-Kraepelinian emphasis on symptoms and diagnosis, and the neo-Kraepelinian era, which also began in the 1970s, was inhospitable to vulnerability research. As neo- Kraepelinian influence waned, vulnerability research accelerated. By the end of the 20th century multiple abnormalities had been identified – in the domains of attention, perception, language, and motor functioning – that are present in individuals with hereditary risk for schizophrenia and in the case of children, that statistically predict later onset of illness. In addition, some childhood disorders, e.g., intellectual disability (mental retardation in older terminologies), attention deficit hyperactivity disorder (ADHD), and autism, are also associated with a heightened probability of schizophrenia in adulthood. Research also began to address another paradox not addressed by the Meehl-Zubin perspective: The vulnerability is not specific to schizophrenia. It generalizes beyond schizophrenia to other psychiatric disorders, even alcoholism. This realization led to our current concepts of neurodevelopmental disorders and the schizophrenia spectrum.
Psychological abnormalities hypothesized to be hereditary vulnerabilities for mental illness came to be known as endophenotypes, phenotypes observable only through special methods (e.g., psychological tests). Today much of the research on the etiology of the schizophrenia spectrum involves a search for endophenotypes, although it is no longer presumed that all psychological vulnerabilities have genetic origins. Consistent with the biosystemic paradigm of modern behavioral neuroscience (see Section 1.1.4), vulnerabilities are identified at genetic, neurophysiological, neuropsychological, cognitive, behavioral and social levels of functioning. The research now generally addresses two key questions:
1. What are the abnormalities that make a person vulnerable to a schizophrenia spectrum disorder and where do they come from?
2. How do vulnerabilities interact to produce the diagnosed disorder?
