Copyright 2012 Aileen M. Echiverri-Cohen - University of Washington

INTRODUCTION
Failure of inhibitory processes involved in the voluntary suppression of information (i.e.,
stimuli classified as irrelevant for an ongoing task; Harnishfeger & Bjorklund, 1993;
Harnishbeger, 1995) have been implicated in the development, maintenance, and treatment of
posttraumatic stress disorder (PTSD; Vasterling, Duke, Brailey, Constans, Allain & Sutker,
2002). Given that preliminary work suggests that treatment recovery is associated with
improvement in cognitive deficits in inhibition (e.g., Vermetten, Vythilingam, Southwick,
Charney, & Bremner, 2003), treatment outcome in PTSD should be related to measures of
inhibition; however, no study has directly examined this relationship.
Many researchers and theorists (e.g., Blechert, Michael, Vriends, Margraf, & Wilhelm,
2007; Rothbaum & Davis, 2003) conceptualize PTSD as an overgeneralization of stress
responding to non-fearful stimuli. Although pre-existing inhibitory deficits may increase the
likelihood of this overgeneralization, over time this overgeneralization may lead to a breakdown
of inhibitory processes associated with executive functioning (Bremner et al., 1993; Sutker,
Davis, Mark, Uddo, & Ditta, 1995). Specifically, there is accumulating evidence from
neuroimaging studies that the medial prefrontal cortex (mPFC) assumes an inhibitory role in
emotion and cognition (Whalen et al., 1998; Bush, Luu, & Posner, 2000, Kerns, Cohen,
MacDonald, Cho, Stenger, & Carter, 2004). PTSD is characterized by functional abnormalities
between the mPFC and amygdala (Gilboa et al., 2004; Lanius et al., 2001). Specifically, reduced
activity in the mPFC and greater activity in the amygdala in PTSD is thought to reflect a
potential failure of the mPFC to inhibit an overactivated amygdala (e.g., Morgan, Grillon,
Southwick, Davis, & Charney, 1996; Bremner, Narayan, Staib, Southwick, McGlashan, &
Charney, 1999; Quirk & Beer, 2006). Thus, abnormalities in the functional relationship of these
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