Biological peripheral correlates of anxiety

Anxiety is often accompanied by physiological and neuroendocrine changes in both psychiatric patients and normal volunteers. Among these correlates the increase of plasma cortisol and catecholamine concentrations have also been documented in stress and hyperarousal states and, therefore, their specificity in anxiety remains to be studied. Recent studies have shown that biological correlates of central noradrenergic system activity, measured in the CSF or blood are increased in relation to anxiety symptoms. Redmond (1979) has proposed a model for the study of anxiety based upon the function of the noradrenergic locus coeruleus (LC) which may provide a neuroanatomical basis for these changes. In the animal, electrical and pharmacological activation of the LC causes increased NE turnover and fear-associated behaviors, whereas lesions and pharmacologic inhibition of the LC produce decreased fear-associated behavior and NE turnover. Drugs with known antianxiety efficacy in man decrease the LC firing in animals. In contrast, clonidine, an alpha-2 adrenergic agonist which inhibits LC activity in animals may have antianxiety effects in patients with depression, anxiety, and opiate abstinence syndrome.