Anxiety disorders and agoraphobic symptoms have had a long history: For more than a century they have been the subject of clinical and theoretical interest in psychiatry (Da Costa, 1871; Freud, 1924). Today, through the application of rigorous diagnostic procedures, anxiety has been recognized as an epidemiologically significant disorder, especially in women (Pitts, 1971; American Psychiatric Association, 1980; Robins et al., 1984).
In recent years most research has focused on the possible underlying mechanisms of anxiety. Genetic and endocrinological explanations, particularly the finding that sodium lactate and carbon dioxide precipitate panic attacks, stimulated the rapidly advancing search for metabolic or biological factors (Pitts & McClure, 1967; Marks & Herst, 1970; Crowe et al., 1980; Appleby et al., 1981; Sheehan et al., 1981; van den Hout & Griez, 1984a, b). Nevertheless, a mechanism underlying anxiety that accounts for all cases is still debated, and exact behavioral and phenomenological descriptions of anxiety phenomena are generally lacking. A precise description of the symptomatology and the variability of anxiety over time and place that could further be linked to the growing biological data base is necessary.
Recent advances in the field support this suggestion: Hibbert (1984), Borkovec (1985), and Ley (1985) have offered behavioral, dynamic, affective, and ideational descriptions of anxiety and panic. Ambulatory monitoring of physiological measures has demonstrated that periods of anxiety in normal subjects are phenomenologically similar to spontaneous and situational panic attacks in patients (Margraf et al., 1987) and both are subject to diurnal and situational influences (Freedman et al., 1985; Taylor et al., 1986).