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The late positive potential (LPP) and functional magnetic resonance imaging (fMRI) blood-oxygen-level dependent (BOLD) activity can provide complementary measures of the processing of affective and social stimuli. Separate lines of research using these measures have often employed the same stimuli, paradigms and samples; however, there remains relatively little understanding of the way in which individual differences in one of these measures relates to the other, and all prior research has been conducted in psychiatrically healthy samples and using emotional scenes (not faces). Here, 32 combat-exposed U.S. military veterans with varying levels of post-traumatic stress symptomatology viewed affective social stimuli (angry, fearful and happy faces) and geometric shapes during separate electroencephalographic and fMRI BOLD recordings. Temporospatial principal component analysis was used to quantify the face-elicited LPP in a data-driven manner, prior to conducting whole-brain correlations between resulting positivities and fMRI BOLD elicited by faces. Participants with larger positivities to fearful faces (> shapes) showed increased activation in the amygdala; larger positivities to angry and happy faces (> shapes) were associated with increased BOLD activation in the posterior fusiform gyrus and inferior temporal gyrus, respectively. Across all face types, larger positivities were associated with increased activation in the fusiform "face" area. Correlations using mean area amplitude LPPs showed an association with increased activation in the anterior insula for angry faces (> shapes). LPP-BOLD associations were not moderated by PTSD. Findings provide the first evidence of correspondence between face-elicited LPP and BOLD activation across a range of (normal to disordered) psychiatric health.

Posttraumatic stress disorder (PTSD)—a chronic, debilitating condition, broadly characterized by emotion dysregulation—is prevalent among US military personnel who have returned from Operations Enduring Freedom (OEF) and Iraqi Freedom (OIF). Selective serotonin reuptake inhibitors (SSRIs) are a first-line treatment for PTSD, but treatment mechanisms are unknown and patient response varies. SSRIs may exert their effects by remediating emotion regulatory brain activity and individual differences in patient response might be explained, in part, by pre-treatment differences in neural systems supporting the downregulation of negative affect. Thirty-four OEF/OIF veterans, 17 with PTSD and 17 without PTSD underwent 2 functional magnetic resonance imaging scans 12 weeks apart. At each scan, they performed an emotion regulation task; in the interim, veterans with PTSD were treated with the SSRI, paroxetine. SSRI treatment increased activation in both the left dorsolateral prefrontal cortex (PFC) and supplementary motor area (SMA) during emotion regulation, although only change in the SMA over time occurred in veterans with PTSD and not those without PTSD. Less activation of the right ventrolateral PFC/inferior frontal gyrus during pre-treatment emotion regulation was associated with greater reduction in PTSD symptoms with SSRI treatment, irrespective of pre-treatment severity. Patients with the least recruitment of prefrontal emotion regulatory brain regions may benefit most from treatment with SSRIs, which appear to augment activity in these regions.

Posttraumatic stress disorder (PTSD) – a debilitating disorder characterized by severe deficits in emotion regulation – is prevalent among U.S. military veterans. Research into the pathophysiology of PTSD has focused primarily on emotional reactivity, showing evidence of heightened neural response during negative affect provocation. By comparison, studies of brain functioning during the voluntary regulation of negative affect are limited. In the current study, combat-exposed U.S. military veterans with (n = 25) and without (n = 25) PTSD performed an emotion regulation task during electroencephalographic (EEG) recording. The late positive potential (LPP) was used as a measure of sustained attention toward, and processing of, negative and neutral pictures, and was scored prior to and after instructions to either maintain or down-regulate emotional response using the strategy of cognitive reappraisal. Results showed that groups did not differ in picture-elicited LPP amplitude either prior to or during cognitive reappraisal; reappraisal reduced the LPP in both groups over time. Time-dependent increases in LPP amplitude as a function of emotional reactivity maintenance were evident in the non-PTSD group only. This latter finding may signal PTSD-related deficits in sustained engagement with emotion-processing over the course of several seconds.

Converging lines of evidence suggest that individuals with comorbid post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) may be characterized by heightened defensive reactivity, which serves to maintain drinking behaviors and anxiety/hyperarousal symptoms. Notably, however, very few studies have directly tested whether individuals with PTSD and AUD exhibit greater defensive reactivity compared with individuals with PTSD without AUD. The aim of the current study was to therefore test this emerging hypothesis by examining individual differences in error related negativity (ERN), an event-related component that is larger among anxious individuals and is thought to reflect defensive reactivity to errors. Participants were sixty-six military veterans who completed a well-validated flanker task known to robustly elicit the ERN. Veterans were comprised of three groups: controls (i.e., no PTSD or AUD), PTSD-AUD (i.e., current PTSD but no AUD), and PTSD+AUD (i.e., current comorbid PTSD and AUD). Results indicated that in general, individuals with PTSD and controls did not differ in ERN amplitude. However, among individuals with PTSD, those with comorbid AUD had significantly larger ERNs than those without AUD. These findings suggest that PTSD+AUD is a neurobiologically unique subtype of PTSD and the comorbidity of AUD may enhance defensive reactivity to errors in individuals with PTSD.