Do Anxiety Patients Differ in Autonomic Base Levels and Stress Response from Normal Controls?

Abstract

During the past decade much attention has been focused on anxiety disorders. Progress has been made with regard to classification, therapy, and psychophysiology and biochemistry of underlying mechanisms. Challenge procedures are the most widely used approach to the biology of anxiety states, especially panic attacks, and have focused on several neurotransmitter systems. Besides the benzodiazepine-GABA-receptor complex (Dorow et al. 1983) and the adenosine receptor (Charney et al. 1985), the adrenergic system turned out to be a very promising one. Drug challenges with yohimbine (Charney et al. 1984, 1987), with isoproterenol (Nesse et al. 1984; Rainey et al. 1984), with lactate (Liebowitz et al. 1984; Fyer et al. 1985), and breathing CO₂ (Gorman et al. 1984) led to the assumption that pharmacologically or physiologically induced changes have a direct panic-inducing effect in anxiety patients, but not in healthy controls. However, these hypotheses are by no means proven. Counterhypotheses have emerged out of the findings of other research groups (Clark and Hensley 1982; van den Hout and Griez 1982; Hippert 1984; Ley 1985; Griez et al. 1986; Margraf et al. 1986; Ehlers et al. 1986). They suggest that panic attacks appear as a result of close interaction of biological factors, experimental setting, expectancy factors, and conditioning mechanisms.