Bouton, M. E., Mineka, S., & Barlow, D. H. (2001). A modern learning theory perspective on the etiology of panic disorder. Psychological Review, 108(1), 4-32.

Several theories of the development of panic disorder (PD) with or without agoraphobia have emerged in the last 2 decades. Early theories that proposed a role for classical conditioning were criticized on several grounds. However, each criticism can be met and rejected when one considers current perspectives on conditioning and associative learning. The authors propose that PD develops because exposure to panic attacks causes the conditioning of anxiety (and sometimes panic) to exteroceptive and interoceptive cues. This process is reflected in a variety of cognitive and behavioral phenomena but fundamentally involves emotional learning that is best accounted for by conditioning principles. Anxiety, an anticipatory emotional state that functions to prepare the individual for the next panic, is different from panic, an emotional state designed to deal with a traumatic event that is already in progress. However, the presence of conditioned anxiety potentiates the next panic, which begins the individual's spiral into PD. Several biological and psychological factors create vulnerabilities by influencing the individual's susceptibility to conditioning. The relationship between the present view and other views is discussed. (PsycINFO Database Record (c) 2000 APA, all rights reserved)

[middle of page 15 of wk 7 handout]

Brewin, C. R. (2001). A cognitive neuroscience account of posttraumatic stress disorder and its treatment. Behaviour Research and Therapy, 39(4), 373-393.

Recent research in the areas of animal conditioning, the neural systems underlying emotion and memory, and the effect of fear on these systems is reviewed. This evidence points to an important distinction between hippocampally-dependent and non- hippocampally- dependent forms of memory that are differentially affected by extreme stress. The cognitive science perspective is related to a recent model of posttraumatic stress disorder, dual representation theory, that also posits separate memory systems underlying vivid reexperiencing versus ordinary autobiographical memories of trauma. This view is compared with other accounts in the literature of traumatic memory processes in PTSD, and the contrasting implications for therapy are discussed. (C) 2001 Elsevier Science Ltd. All rights reserved.(online article)

Mineka, S., & Ohman, A. (2002). Phobias and preparedness: The selective, automatic, and encapsulated nature of fear. Biological Psychiatry, 52(10), 927-937.

We describe evidence for an evolved module for fear elicitation and fear learning with four primary characteristics. First, it is preferentially activated by stimuli related to survival threats in evolutionary history. Thus, fear-relevant stimuli lead to superior conditioning of aversive associations compared with fear-irrelevant stimuli. Second, the module is automatically activated by fear- relevant stimuli, meaning that fear activation occurs before conscious cognitive analysis of the stimulus can occur. Third, the fear module is relatively impenetrable to conscious cognitive control, and fear conditioning with fear-relevant stimuli can occur even with subliminal conditioned stimuli. Fourth, the amygdala seems to be the central brain area dedicated to the fear module. Finally, we propose that there are two levels of fear conditioning, with an emotional level that is relatively independent of the cognitive contingency level, each mediated by different brain areas. (C) 2002 Society of Biological Psychiatry.

Mineka, S., & Zinbarg, R. (1996). Conditioning and ethological models of anxiety disorders: Stress-in-Dynamic-Context Anxiety models, In Hope, Debra A. (Ed). (1996). Nebraska Symposium on Motivation, 1995: Perspectives on anxiety, panic, and fear. Current theory and research in motivation, Vol. 43. (pp. 135 210). Lincoln, NE, US: University of Nebraska Press.

(from the chapter) argue that the central shortcoming of traditional behavioral models has been their failure to consider the dynamic context in which stressors occur in a person's life / by ignoring the powerful effect of dynamic contextual factors on the impact of those stressors, behavioral models have appeared to be much more simplistic than they need to be and to have far less explanatory power than we know they can have / refer to the more traditional models as Stress- in-Total-Isolation Anxiety models (SITIA models) / present an alternative model in which we show that stress must always be considered in a dynamic context rather than in isolation in determining the outcome of exposure to stress /// the relevant dynamic contextual factors that we will consider include constitutional factors such as temperament, past experiential history (including general factors such as a history of exposure to uncontrollable life events as well as specific factors such as prior traumatic conditioning events), current contextual factors at the time of a stressor (such as whether there are already reliable predictors of the stressor, or the nature of the conditioned stimulus relative to the nature of the unconditioned stimulus, or whether the stressor can be controlled), and future modification of the impact of the stressor (through processes such as forgetting and other memory modifications, as well as through later experiences with other stressors) / refer to these models as the Stress-in-Dynamic-Context Anxiety models (SIDCA models) /// specific phobias [vicarious conditioning of fears and phobias, sources of individual differences in the acquisition of fears and phobias, selective associations in the conditioning of fears and phobias, persistence of fears and phobias] / social phobia [preparedness and conditioning models of social phobia; direct traumatic conditioning, observational conditioning, and social phobia; temperamental variables and social phobia; uncontrollability and social phobia] / panic disorder and agoraphobia / generalized anxiety disorder / posttraumatic stress disorder (PTSD) / obsessive-compulsive disorder [animal models of compulsive behaviors, anxiety reduction theory, preparedness and the nonrandom distribution of obsessive thoughts and compulsive behaviors] (PsycINFO Database Record (c) 2000 APA, all rights reserved)

Ohman, A., & Mineka, S. (2001). Fears, phobias, and preparedness: Toward an evolved module of fear and fear learning. Psychological Review, 108(3), 483-522.

An evolved module for fear elicitation and fear learning with 4 characteristics is proposed. (a) The fear module is preferentially activated in aversive contexts by stimuli that are fear relevant in an evolutionary perspective. (b) Its activation to such stimuli is automatic. (c) It is relatively impenetrable to cognitive control. (d) It originates in a dedicated neural circuitry, centered on the amygdala. Evidence supporting these propositions is reviewed from conditioning studies, both in humans and in monkeys; illusory correlation studies; studies using unreportable stimuli; and studies from animal neuroscience. The fear module is assumed to mediate an emotional level of fear learning that is relatively independent and dissociable from cognitive learning of stimulus relationships.

Otto, M. W. (2002). Learning and "unlearning" fears: Preparedness, neural pathways, and patients. Biological Psychiatry, 52(10), 917-920. (electronic only via ScienceDirect).

Given the dramatic success of exposure-based treatments for the anxiety disorders, it is not surprising that clinical procedures advanced separately from developments in extinction research in animal laboratories. Bridging this gap between clinical and animal researchers was a major goal of the Satellite Symposium for the 2002 Anxiety Disorders Association of America (ADAA) conference. The title of the symposium, "Learning and `Unlearning' Fears: Preparedness, Neural Pathways, and Patients," reflects the consideration of this topic from evolutionary, neuroanatomic, learning, and clinical perspectives. This symposium was sponsored jointly by the ADAA, the ADAA Scientific Advisory Board, and the National Institute of Mental Health, and was supported by an unrestricted educational grant to the ADAA from Wyeth Pharmaceuticals.
Symposium speakers were selected to address questions regarding the systems, structures, and events that influence the ease with which fears are learned in the first place, and the implications these factors may have for the subsequent relearning of safety. Perspectives were provided on preparedness for fear learning, including discussion of markers of risk for anxiety disorders and the potential impact of early, corrective experiences on individuals with these markers. Likewise, the process of extinction was considered from the standpoint of contextual effects on learning and the neural pathways involved in this process. The role of pharmacologic agents in changing the context for extinction was also considered, and the symposium closed with discussion of the implications of some of these issues for pharmacotherapy, cognitive-behavior therapy, and their combination.