Future pharmacotherapy for post-traumatic stress disorder: prevention and treatment.
I have presented two complementary lines of speculation in this article. First, I have presented a public health model of resilience, prevention, acute intervention, and tertiary treatment to inform a pharmacotherapeutic strategy for PTSD in the future. Second, I have proposed a rational rather than an empirical approach to the clinical pharmacology of PTSD. Such an approach suggests that efforts be directed toward the development and testing of new classes of drugs designed to target the unique pathophysiology of PTSD.
Friedman
Matthew J
MJ
National Center for PTSD, VAM ROC 116D, 215 N. Main Street, White River Junction, VT 05009-0001, USA. matthew.friedman@dartmaith.edu
D018663:Adrenergic Agents / Q000627:therapeutic use; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D009478:Neuropeptide Y / Q000037:antagonists & inhibitors; D018377:Neurotransmitter Agents / Q000378:metabolism; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D018019:Receptors, Corticotropin-Releasing Hormone / Q000378:metabolism; D011957:Receptors, Opioid / Q000187:drug effects; D013313:Stress Disorders, Post-Traumatic / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D013315:Stress, Psychological / Q000188:drug therapy / Q000503:physiopathology
D018663:Adrenergic Agents; D009478:Neuropeptide Y; D018377:Neurotransmitter Agents; D018019:Receptors, Corticotropin-Releasing Hormone; D011957:Receptors, Opioid; D018698:Glutamic Acid