Psychiatric Pathophysiology: Anxiety Disorders
One thing is certain, that the problem of anxiety is a nodal point, linking up all kinds of important questions: a riddle, of which the solution must cast a flood of light upon our whole mental life.
In the 50 years since DSM-I, the rubric of “anxiety disorder’’ has evolved and expanded to encompass generalized anxiety disorder (GAD), panic disorder (PD), phobias, obsessive–compulsive dis-order (OCD) and post traumatic stress disorder (PTSD) (Rickels and Rynn, 2001). Given the complex circuitry required to in-tegrate behaviors characteristic of the anxiety disorders (Lang et al., 1998; Coplan and Lydiard, 1998; Davis 1998), it seems implausible that a single gene product or transmitter system will ultimately be identified as the sole mediator of any anxiety disorder.
Most contemporary neurobiological theories of anxiety dis-orders are grounded on the molecular mechanisms of drugs used to treat these disorders. Despite the ever-increasing use of geneti-cally engineered mice (which has certainly added to our knowledge base), this “reverse engineering’’ approach remains the standard in biological psychiatry, in part because of the difficulties inherent in validating animal models of psychiatric disorders. Further, when a drug is shown to be effective, variants of the drug (differing in potency and/or efficacy) often facilitate hypothesis testing in both animals and humans.