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.

Research on relationships between anxiety and depression has proceeded at a rapid pace since the 1980s. The similarities and differences between these two conditions, as well as many of the important features of the comorbidity of these disorders, are well understood. The genotypic structure of anxiety and depression is also fairly well documented. Generalized anxiety and major depression share a common genetic diathesis, but the anxiety disorders themselves are genetically hetergeneous. Sophisticated phenotypic models have also emerged, with data converging on an integrative hierarchical model of mood and anxiety disorders in which each individual syndrome contains both a common and a unique component. Finally, considerable progress has been made in understanding cognitive aspects of these disorders. This work has focused on both the cognitive content of anxiety and depression and on the effects that anxiety and depression have on information processing for mood-congruent material.

Trait concepts are used extensively in psychopathology research, but much of this research has failed to consider recent advances in the dimensional structure of personality. Many investigators have discounted the importance of this structural research, arguing that (a) little progress has been made in this area, (b) structural models have little direct relevance for psychopathology research, and (c) the principal methodological tool of structural research--factor analysis--is too subjective to yield psychologically meaningful results. We dispute each of these objections. Specifically, we offer an integrative hierarchical model--composed of four higher order traits--that is congruent with each of the major structural subtraditions within personality. We also discuss the implications of this integrative scheme for basic trait research, for the conceptualization and assessment of psychopathology, and for the etiology of disorder.

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, particularly those that emphasize the role of catastrophic misinterpretation of somatic sensations, is discussed.

The authors describe how contemporary learning theory and research provide the basis for perspectives on the etiology and maintenance of anxiety disorders that capture the complexity associated with individual differences in the development and course of these disorders. These insights from modern research on learning overcome the shortcomings of earlier overly simplistic behavioral approaches, which sometimes have been justifiably criticized. The authors show how considerations of early learning histories and temperamental vulnerabilities affect the short- and long-term outcomes of experiences with stressful events. They also demonstrate how contextual variables during and following stressful learning events affect the course of anxiety disorder symptoms once they develop. This range of variables can lead to a rich and nuanced understanding of the etiology and course of anxiety disorders.