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

shown to modify attentional processes (Nakatani, Baijal, & van Leeuwen, 2009). This
explanation cannot be ruled out without a control or waitlist group as part of the study design.
Better inhibitory functioning on PPI was associated with better treatment response,
suggesting that better prepulse inhibition may be a potential biomarker for treatment response.
The size of the effects here were large but the findings were at a trend level probably due to
sample size. Indeed, identifying biomarkers are a promising approach to understanding disorders
and treatment response (Deutsch et al., 2009; Ritsner & Gottesman, 2009; Van Lieshout &
Szatmari, 2009). Biomarkers are measureable indicators of a biological process that is directly
linked to the clinical manifestation of a disorder (Beauchaine; 2009; Ritsner et al., 2009).
According to this definition, for PPI to qualify as a biomarker, measurable deficits in this tasks
must be linked to an identifiable abnormal neural network and associated with the
pathophysiology of PTSD.
The present study examined inhibitory failures in basic processes of sensory gating
processes (Graham, 1975; 1979; Filion, Dawson, & Schell, 1998; Fendt, Li, Yeomans, 2001) that
purportedly result from disruptions in the fear circuitry in PTSD (Kolb, 1987; Morgan, Grillon,
Lubin & Southwick, 1997). Thus, inhibitory deficits measured by PPI presume a common
biological basis of a disrupted neural circuitry involving the prefrontal regions and amygdala
(Campeau and Davis, 1995; Hitchcock and David, 1996; Fendt et al., 2001). Abnormalities in
PPI show close associations to PTSD symptoms, with abnormal PPI, or disturbances in early
sensory flooding, being implicated in PTSD (Grillon et al., 1998; Ornitz et al., 1989). As there
are few studies that have examined biomarkers of treatment recovery, the findings are
preliminary and need further replication. Taken together, better PPI may represent a potential
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