Objective: Attentional inhibitory deficits expressed as difficulty ignoring irrelevant stimuli in the pursuit of goal-directed behavior may serve as a fundamental mechanism of posttraumatic stress disorder (PTSD). Evidence of inhibitory processes as central to extinction suggests that exposure-based treatments may act more directly on the inhibitory deficits implicated in PTSD, whereas, in facilitating serotonergic neurotransmission, selective serotonin reuptake inhibitors (SSRIs) may be less direct and bring about general neurochemical changes in the fear circuitry. If these inhibitory deficits underlie PTSD, then inhibition should improve with successful treatment, with those treated with prolonged exposure (PE) potentially resulting in greater changes in inhibition than those treated with sertraline.
Method: Changes in temporal attentional inhibition, using an attentional blink (AB) paradigm, were examined at pre- and posttreatment in 49 individuals (74.5% female, 66.7% Caucasian, age M = 37.69, SD = 12.8 years) with chronic PTSD. Participants completed 10 weeks of either PE or sertraline.
Results: Individuals who made greater improvements with PE showed faster improvements in temporal inhibition on the critical inhibitory lag of AB than those who made greater improvements with sertraline (d = 0.94). These changes could not be accounted for by basic attention.
Conclusions: Greater improvement in fundamental attentional inhibitory processes with better treatment response to PE, compared with sertraline, suggests potential specificity in how PTSD treatments normalize inhibitory processes, such that exposure-based treatments like PE may target inhibitory processes and improve basic inhibitory functioning.
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