Student presents, "The Hole Isn’t Round: Why Pharmacotherapy for PTSD Often Doesn’t Fit" at Fielding's Winter Session 2013

Ann Trotter, Fielding's School of Psychology

The neurobiology of chronic PTSD is essential to targeting effective pharmacologic treatment and the development of new medications. Individuals who develop chronic PTSD often suffer severe symptoms to the point of incapacitation; exhibit marital, social/relational, and/or vocational impairment; and use a disproportionate amount of community psychiatric and medical services (Foa, et al., 2009). The pathophysiology of chronic PTSD is thought to arise from the inability of neurobiological systems to adapt to severe stressors. Alterations in mechanisms of learning and extinction, increased sensitization to stress, and increased physiological arousal appear to develop as a result (Heim & Nemeroff, 2009). To date, pharmacologic agents utilized in treating PTSD are variably effective in reducing symptom frequency and intensity/severity, and none have been developed to specifically target the neurobiologic systems implicated in chronic PTSD (Stahl, 2008). This poster is a visual guide which outlines the pharmacologic agents used in the treatment of PTSD and highlights the neurobiologic system in which they are thought to exert their primary effects. Classes of drugs such as anticonvulsants, atypical antipsychotics, and ‘novel’ treatments for PTSD, such as mifepristone (RU-486) and MDMA (3,4-Methylenedioxymethamphetamine) are highlighted.