Clinical correlates of attentional bias to drug cues associated with cocaine dependence.

BACKGROUND AND OBJECTIVE: Preoccupation (attentional bias) related to drug-related stimuli has been consistently observed for drug-dependent persons with several studies reporting an association of the magnitude of measured attentional bias with treatment outcomes. The major goal of the present study was to determine if pre-treatment attentional bias to personal drug use reminders in an addiction Stroop task predicts relapse in treatment-seeking, cocaine-dependent subjects. METHODS: We sought to maximize the potential of attentional bias as a marker of risk for relapse by incorporating individualized rather than generalized drug use cues to reflect the personal conditioned associations that form the incentive motivation properties of drug cues in a sample of cocaine-dependent subjects (N = 35). RESULTS: Although a significant group Stroop interference effect was present for drug versus neutral stimuli (ie, attentional bias), the level of attentional bias for cocaine-use words was not predictive of eventual relapse in this sample (d = .56). A similar lack of prediction power was observed for a non-drug counting word Stroop task as a significant interference effect was detected but did not predict relapse outcomes (d = .40). CONCLUSIONS AND SCIENTIFIC SIGNIFICANCE: The results of the present study do not provide clear support for the predictive value of individual variation in drug-related attentional bias to forecast probability of relapse in cocaine-dependent men.

C-reactive protein moderates associations between racial discrimination and ventromedial prefrontal cortex activation during attention to threat in Black American women.

Prior research has shown that racial discrimination (RD) impacts activation in threat network regions, including the ventromedial prefrontal cortex (vmPFC) and middle occipital cortex during attention to threat-relevant stimuli. However, little is known about the biological mechanisms that may modulate these effects; inflammation may be a pathway linking RD and threat network activation. As such, the current study aimed to explore whether systemic inflammation, measured by C-reactive protein (CRP) levels, may moderate the relationship between RD and activation in the vmPFC and middle occipital cortex during attention to threat. Blood samples for inflammatory marker (CRP) assays were obtained from forty Black American women (mean [SD] age, 39.93 [9.97] years; range, 22-58 years) recruited from an ongoing trauma study; participants also viewed threat-relevant stimuli as part of an attention task during fMRI. We found that CRP moderated the relationship between RD and vmPFC activation during attention to threat, such that participants with relatively higher concentrations of CRP ( ≥ 23.97 mg/L) demonstrated significant positive associations between RD and vmPFC activation [ß = 0.18, CI (0.04, 0.32), t = 2.65, p = 0.01]. No significant associations were observed for participants who showed moderate (10.89 mg/L) or low (0.20 mg/L) CRP concentrations. CRP did not moderate the relationship between RD and middle occipital cortex activation. Our data present a mechanism through which RD may influence immune system activation and, in turn, threat network activation. Inflammation may contribute to brain health vulnerabilities in Black Americans via its effects on threat circuits; this merits further investigation in large-scale studies.

Attentional control abnormalities in posttraumatic stress disorder: Functional, behavioral, and structural correlates.

BACKGROUND: Attentional disruptions are common in PTSD, but findings across neuropsychological and neuroimaging studies have been variable. Few PTSD studies have investigated abnormalities in attention networks using a multi-modal imaging approach and attentional tasks that include emotionally-salient images. This study combined a behavioral task that included these images (emotional Stroop) with functional and structural neuroimaging (fMRI and diffusion tensor imaging; DTI) methods to comprehensively investigate attentional control abnormalities in a highly-traumatized civilian sample. METHODS: 48 traumatized women with and without PTSD received clinical assessments, fMRI and DTI. During fMRI, the Affective Stroop (AS), an attentional control task that includes emotionally-salient distractor images (trauma-relevant, positive, neutral) and variable task demands, was administered. RESULTS: In response to more difficult AS trials, participants with PTSD demonstrated lower activation in the dorsal and rostral anterior cingulate cortex and greater activation in the insula. This group also showed comparatively poorer performance on positive AS distractor trials, even after adjusting for trauma exposure. Performance on these trials inversely correlated with structural integrity of the cingulum bundle and uncinate fasciculus. CONCLUSIONS: Even after adjusting for trauma exposure, participants with PTSD showed worse performance on an attentional control task in the context of emotional stimuli. They also showed relatively lower cognitive control network activation and greater salience network activation. Fronto-parietal and fronto-limbic white matter connectivity corresponded with AS performance. Our findings indicate that attentional control impairments in PTSD are most evident in the context of emotional cues, and are related to decrements in function and structure of cognitive control and salience networks.

Reduced neural activation during an inhibition task is associated with impaired fear inhibition in a traumatized civilian sample.

INTRODUCTION: Impaired inhibition of fear in the presence of safety cues and a deficiency in the extinction of fear cues are increasingly thought to be important biological markers of Posttraumatic stress disorder (PTSD). Other studies have suggested that there may be altered neural activation during behavioral inhibition tasks in subjects with PTSD. The current study aimed to see whether neural activation during inhibition was reduced in a highly traumatized civilian population, and whether atypical activation was associated with impaired fear inhibition. METHODS: The participants were 41 traumatized women (20 PTSD+, 21 PTSD-) recruited from Grady Memorial Hospital in Atlanta, GA. We used a Go/NoGo procedure with functional magnetic resonance imaging (fMRI) in a high-resolution 3T scanner. Participants were instructed to press a button whenever an "X" or "O" appeared on the screen, but not if a red square appeared behind the letter. Participants were assessed for trauma history and PTSD diagnosis, and completed a fear-potentiated startle and extinction paradigm. RESULTS: We found stronger activation in the ventromedial prefrontal cortex (vmPFC) in traumatized subjects without PTSD compared to those with PTSD in the NoGo greater than Go contrast condition. Activation in the vmPFC was negatively correlated with fear-potentiated startle responses during safety signal learning (p = .02) and fear extinction (p = .0002). CONCLUSIONS: These results contribute to understanding of how the neural circuitry involved in inhibitory processes may be deficient in PTSD. Furthermore, the same circuits involved in behavioral inhibition appear to be involved in fear inhibition processes during differential fear conditioning and extinction.