Über die Autorin bzw. den Autor

Bruce F. Pennington, PhD, is John Evans Professor of Psychology at the University of Denver, where he heads the Developmental Cognitive Neuroscience program. He received his BA in English at Harvard University in 1968 and his PhD in Clinical Psychology at Duke University in 1977. He has earned an international reputation for his research on dyslexia, autism, and attention-deficit/hyperactivity disorder, and has published over 150 scientific papers on these topics. His honors include Research Scientist, MERIT, and Fogarty awards from the National Institutes of Health. Dr. Pennington's earlier book, Diagnosing Learning Disorders, emphasizes a close relation between research and practice. In addition to being a researcher and research mentor, he is also a child clinical neuropsychologist and has been active in clinical practice and training throughout his career.
.

Auszug. © Genehmigter Nachdruck. Alle Rechte vorbehalten.

The Development of Psychopathology

Guilford Publications

Chapter One

This chapter first considers the need for a framework to integrate the various levels of analysis necessary for understanding the development of a psychopathology. Such a framework raises a key issue: the mind-body problem in psychopathology. After examining this issue, we turn to the use and validation of diagnoses, and conclude with fallacies that have impeded understanding of this difficult topic.

ECUMENISM VERSUS INTEGRATION: THE NEED FOR A NEW FRAMEWORK

Despite considerable empirical progress in the field of psychopathology in the last few decades, we lack a satisfactory comprehensive theory. The 20th century began with a comprehensive theory of psychopathology, Freud's psychoanalytic theory, which dominated the field for at least 50 years. Its focus on the importance of early relationships and development are still important insights, and are still being investigated by attachment theorists. Psychoanalysis as a treatment has evolved into interpersonal forms of psychotherapy, some of which are empirically validated. Yet psychoanalytic theory's shortcomings as a scientific explanation of psychopathologies are now well known. Within psychology, psychoanalytic theory was replaced by learning and then by cognitive-behavioral theories of psychopathology. Within psychiatry, Freudian theory has largely been replaced by biological psychiatry. But neither biological psychiatry nor cognitive-behavioral psychology offers a comprehensive theory for understanding psychopathology.

Biological psychiatry has the advantage of placing the brain squarely in the center of the understanding of psychopathology, but it often has been too reductionistic: too focused on single causes (e.g., alterations in a given neurotransmitter) or on a single level of analysis (e.g., synapses).

Current psychological theories have the advantage of dealing with interpersonal and social contexts that shape the development of a psychopathology, but they are weak at explaining individual differences and mostly ignore the brain.

This state of affairs is often reflected in contemporary abnormal psychology or psychiatry books by an uneasy ecumenism. Psychological and physiological theories are laid out side by side but rarely integrated. Some texts speak of a "biopsychosocial" model, but this model is usually an ecumenical umbrella for covering disparate approaches rather than an integration.

So we are at an interesting point in the history of the science of psychopathology. Previous comprehensive theoretical paradigms have failed; new empirical methods are rapidly producing data that need to be accounted for, but current theories of psychopathology are inadequate for the task of integration. At the same time, a new scientific paradigm is emerging in cognitive neuroscience. However, to deal with the development of psychopathology, cognitive neuroscience needs to be broadened in three key ways: (1) It must focus explicitly on individual differences; (2) it must integrate emotion and social influences into the study of cognition; and (3) it must incorporate development. Although this book does not pretend to offer a complete new theory of psychopathology, it does attempt to lay out the conceptual and empirical constraints that a new theory of psychopathology will have to meet, and to show how a cognitive neuroscientific approach can satisfy those constraints.

Hence, a basic message of this book is that we need a way to integrate research on the biological and psychological mechanisms involved in developmental psychopathologies. Consider a child with mild depression, or dysthymia. A biologist might seek the explanation for this clinical condition in differences in receptors for neurotransmitters. But a psychologist might seek the explanation in differences in attachment security. These very different ways of thinking about the same clinical phenomenon are not necessarily competing explanations. Rather, they may be complementary, each operating at a different level of analysis. However, for either the biologist or the psychologist to think about how these two explanations relate to each other is not straightforward because a theoretical framework for integrating these different levels of explanation is only beginning to emerge.

This neuroscientific framework seeks to relate behavior and mind to the brain. It is important to realize that every psychopathology requires us to solve the brain-behavior or mind-body problem. It is not enough to frame an explanation of a psychopathology purely in terms of mental or psychological constructs. To do so ignores the brain. At the same time, to frame an explanation purely in terms of brain variables such as receptor efficiencies or densities is not enough. To do so reveals a naive reductionism, because even if the causal brain variables were known, we would still need to know how these brain differences lead to changes in behavior.

The important overall point of a neuroscientific perspective is that analyses of normal or abnormal function need to be informed by an understanding of the brain structures and processes that implement the function. In other words, "hardware" matters and provides important constraints for developmental theories, whether they are theories of neo-Piagetian cognitive operations or internal working models in attachment theory. So taking a neuroscientific perspective forces us to confront a latent "dualism" in much of developmental psychology, the assumption that analyses of behavioral function can proceed completely independently of analyses of brain. As Patricia Goldman-Rakic (1987a) aptly said in discussing the relation between neuroscience and developmental psychology, "The 'empty organism' has long since been filled with intentionality and information-processing skills, but not necessarily with a central nervous system" (p. 601).

To draw out the implications of this point, let us take as an example a hypothetical developmental psychopathology that is entirely determined by the social (i.e., interpersonal) environment-no genetic influence; no traumatic, toxic, or other noninterpersonal environmental alteration of brain development. It is very easy to catch oneself thinking that in such a case the pathogenetic social influences are registered somewhere other than the brain-in the attachment system, in object relations, or what have you. The point of a neuroscientific perspective is that all social influences affect brain development in some way or another, and all psychological constructs are implemented by brain mechanisms. For instance, the neuropsychology of traumatic social experiences such as loss, neglect, and abuse is becoming fairly well understood. Such traumas can cause very persistent changes in brain development. Moreover, positive social experiences also affect brain development and function. Humans are social animals and are therefore "open" systems, dependent on social relations. So taking a neuroscientific perspective does not limit the unit of analysis to an individual person (or his or her nervous system). Psychopathology may exist in an individual, a dyad, or a social group; I am simply arguing that a neuroscientific perspective is relevant in each case. For instance, it has been shown that an individual baboon's neurochemistry changes when its position in the dominance hierarchy changes (Sapolsky, 1994).

These considerations mean that the familiar clinical distinction between "functional" and "organic" is misleading and, in a strict sense, fundamentally incorrect. There is no autonomous substrate for functional pathologies, nor does the functional-organic distinction neatly divide disorders either by treatability or mode of treatment. For instance, it is frequently assumed that functional disorders call for behavioral treatments and are more amenable to treatment, whereas organic ones are less treatable and call for biological interventions. However, many counterexamples, such as phenylketonuria (PKU) on the one hand, and multiple personality disorder on the other, can be cited.

One can discern this functional versus organic assumption in contemporary psychopathology textbooks. The most heritable disorders, such as bipolar illness or autism, are thought of as "biological" disorders, whereas less heritable disorders, such as dysthymia or phobias, are thought of as functional disorders produced by socialization or experience. As we will see, there is a striking absence of psychological theories for the development of bipolar disorder and fewer psychological treatments. Also, the success of early psychological treatments for autism questions this assumption. The main point is that as soon as we accept this assumption, we have given up on a universal theory of psychopathology.

It is also important to emphasize that a commitment to a neuroscientific perspective does not commit one to a belief in single, deterministic causes for developmental psychopathology. Developmental psychopathologies are complex behavioral disorders in two senses: The disrupted behaviors are complex, and the multiple developmental pathways that led to the disruption are complex. For most psychopathologies, multiple risk and protective factors, both genetic and environmental, affect outcome in a probabilistic rather than deterministic fashion. Both normal and abnormal development result from the self-organizing properties of complex systems, so single causes are unlikely, and interactions and nonlinearities are to be expected.

So, clearly, my point about the relevance of brain mechanisms for understanding a purely social pathology is not an argument for reductionism. Risk factors will be found at different levels of analysis for different developmental psychopathologies: the molecular level for some, and the attachment system for others. But all risk factors act on the same complex developmental system that cannot be eliminated from an explanation. Thus, no level of analysis is entirely autonomous or encapsulated; interpersonal systems do not exist in some "social ether" outside of human organisms. Learning and using such systems is constrained by the real human brain, which evolved for just that function, among others. Moreover, dynamic principles that describe network properties within a brain may well have some utility in describing the dynamics of social networks.

Our claims about the relevance of neuroscience for purely social pathologies are integrative rather than reductionistic. The point is that neuroscience potentially provides a broad-enough paradigm to encompass all of developmental psychopathology. While a complete explanation for some pathologies may emphasize different levels of analysis than the explanation of others, all can (and need to) fit within the same broad paradigm. A pathology that is caused in part by genetic influences will require an explanation that begins at the deepest explanatory level, with an altered DNA sequence, and proceeds across many levels of analysis, up to the level of observable behavior. In contrast, a pathology that is completely caused by aberrant parenting may require fewer levels of analysis, but these levels will overlap with those used in the previous example; we should not have to invoke a totally different paradigm. Moreover, aberrant parenting may change gene expression and brain development.

In summary, the argument is that we need a new framework or paradigm for understanding the development of psychopathology, and cognitive neuroscience provides that framework. As discussed by O'Reilly and Munakata (2000), there are two complementary aspects of a cognitive neuroscience approach: physical reductionism and reconstructionism. Both aspects are needed for a comprehensive understanding of psychopathology. Unlike most contemporary psychological theories of psychopathology (e.g., cognitive-behavioral or developmental theories), cognitive neuroscience is explicitly committed to physical reductionism: The components of cognition and behavior must be reduced to their physical substrate, the brain, just as key aspects of living organisms have been reduced to molecular biology. Biological psychiatry has applied physical reductionism to psychopathology with noteworthy success, but physical reductionism alone cannot give us an explanation of complex behavior. Unlike much of biological psychiatry, cognitive neuroscience is also explicitly committed to reconstructionism: an account of how interactions among the elementary units (i.e., neurons) of the nervous system give rise to the phenomena of cognition and behavior. Achieving this reconstruction has been greatly aided by the development of neural network models, which, as we will see, have provided a much deeper functional understanding of how complex cognitive phenomena arise from the interaction of neuron-like elements. (But, unfortunately, there are relatively few neural network models of psychopathology.) In short, current approaches to psychopathology are either functional theories unrelated to the brain or biological reductions that do not attempt to reconstruct function. Although both approaches have made empirical progress and have led to the development of effective treatments, they cannot by themselves be integrated. A different framework is needed to accomplish that, one that includes both physical reductionism and reconstructionism.

Applying a cognitive neuroscientific approach to psychopathology will enrich both fields and change the boundaries of what we currently consider to be psychopathology. We have just discussed how the field of psychopathology will be enriched. One benefit to cognitive neuroscience is that it will have to include emotion and arousal in its models. As we will see, there is a notable paucity of neural network models of mood and anxiety disorders. In terms of boundaries, the current artificial division between psychiatric and neurological disorders reflects the misleading functional versus organic distinction discussed earlier. For example, some developmental disorders, such as dyslexia and mental retardation, are not always considered psychopathologies. Some neurological disorders, such as attentional neglect or the alien hand syndrome, are virtually never considered psychopathologies. This artificial division exists in spite of the fact that psychopathology is traditionally defined as an alteration in thought, mood, or behavior that impairs adaptive functioning; clearly, developmental and neurological disorders fit this definition. A cognitive neuroscientific approach aspires to explain all these kinds of disorders-traditional psychopathologies, developmental disorders, and neurological disorders-with similar models.



Continues...

Excerpted from The Development of Psychopathologyby Bruce F. Pennington Copyright © 2005 by Bruce F. Pennington. Excerpted by permission.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.