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.
Freud 1917
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.
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