PTSD is associated with low quality of life (Olatunji, Cisler, & Tolin, 2007) and significant psychosocial impairment (Amaya-Jackson et al., 1999; Breslau, 2001; Kessler, 2000). Research has used the EST as one means of elucidating some of the core deficits associated with PTSD (Buckley et al., 2000
; McNally et al., 1990
). Whether an EST effect exists at all in PTSD has been questioned (Kimble et al., 2009
), necessitating a quantitative review to examine the EST effect in PTSD. Further, two complimentary mechanisms are theorized to mediate performance on the EST, a threat detection mechanism and attentional control mechanism, but key EST manipulations that facilitate insights into the mechanisms mediating PTSD have yielded inconsistent results. The present study synthesized this body of literature via meta-analysis as a means of better understanding the core deficits in PTSD.
In regards to the first goal, our quantitative results suggest significantly impaired EST performance in the PTSD group towards PTSD-relevant and generally threatening stimuli, and the EST impairment in the PTSD group is significantly greater than the NTC group. The TC group demonstrated impaired performance towards only PTSD-relevant words, and this impairment was also significantly greater compared to the NTC group. The PTSD and TC groups did not significantly differ in the direct comparisons, though effect sizes consistently favored the PTSD group. On the one hand, the results suggesting that groups only differed in comparisons involving PTSD-relevant words when compared to the NTC group could be interpreted to suggest a lack of an EST effect. That is, trauma-related words are personally relevant to the trauma exposed groups (both TC and PTSD groups) and not the NTC group, so the finding that between group differences are only found towards these words may reflect either an artifact (i.e., personal relevance) or the more general negative consequences of trauma exposure per se (i.e., not PTSD specifically). On the other hand, if it were the case that the observed effects were an artifact of personal relevance, then there should not have been a significant difference between generally threatening words and neutral words (and positive words) found within the PTSD and TC groups. While these effect sizes did not differ significantly between the groups, if it were the case that the observed effects were only due to personal relevance, then there should not have been effects towards non-personally relevant words found only among the clinical groups. Accordingly, the negative consequence of trauma exposure is the most likely interpretation of the present results.
On the one hand, the pattern of results suggesting the negative consequences of trauma exposure generally, and not PTSD specifically, may contradict the hypothesis of an enhanced EST effect in PTSD. That is, if it were the case that PTSD specifically is associated with a pronounced EST effect, then it would be expected that the effects should be greater in PTSD relative to trauma control groups. On the other hand, it is important to consider why comparisons to a trauma control group are important. One factor this comparison controls is personal relevance of the PTSD-words (though not in studies using mixed trauma samples). If personal relevance is held constant between the groups, then differences in performance disruption are likely due to other factors (e.g., attentional control, threat detection). From this perspective, the current results are not consistent with hypotheses of disrupted attentional control or threat detection mechanisms in PTSD. The more obvious factor that a trauma control group comparison controls is trauma exposure, which presumably can address issues of specificity. For example, is psychopathology following trauma exposure uniquely associated with impaired EST performance? From this perspective, the results are again not consistent with the hypothesis that PTSD is uniquely associated with impaired EST performance. However, it is interesting to note that the trauma control group, but not the no trauma control group, had similar within-subject evidence for impaired EST performance. The pattern of within-subject effects and between-group differences suggests that individuals exposed to traumatic events, regardless of PTSD, display impaired EST performance. These findings raise the possibility that the EST effect in PTSD does not necessarily reflect specific characteristics of PTSD; rather, it reflects the consequences of exposure to traumatic events. In a related vein, a growing body of research suggests that assaultive traumas (e.g., combat, physical assault, sexual assault) are a more potent risk factor for PTSD relative to other traumatic event types (e.g., motor vehicle accidents, natural disasters) (Cougle et al., 2009; Resnick et al., 1993). Consistent with the view of impaired EST performance resulting from trauma exposure per se, the present results found that trauma type moderated some of the EST effects in both PTSD and TC groups, such that samples exposed to assault had greater effect sizes relative to other trauma types.
There is a growing body of evidence indicating the negative consequences of traumatic event exposure on both physical health (Sledjeski, Speisman, & Dierker, 2008
) and mental health outcomes (Breslau et al., 1991
; Kilpatrick et al., 2003; Resnick et al., 1993). Relevant to the present topic, emerging research suggests that traumatic event exposure has a cumulative ‘allostatic’ (McEwen, 2004
) effect (Kollassa, Kolassa, Ertl, Papassotiropoulos, & De Quervain, 2010; Neuner et al., 2004; Steel et al., 2009). One study conducted among a sample of over 3000 refugees found that the rate of PTSD was about 23% among individuals exposed to 1–3 traumatic events, and this rate increased up to 100% among individuals exposed to 28 or more traumatic events (Neuner et al., 2004). Neurobiological research is clarifying the mechanisms by which this allostatic effect may occur (Arnsten, 2009
; Izquierdo et al., 2006
; Liston et al., 2006
; Mitra et al., 2005
; Radley et al., 2006
; Vyas et al., 2002
). This research suggests that chronic stress increases dendritic branching in the amygdala and increases reactivity towards motivationally salient cues (e.g., threat cues), and also decreases dendritic spine density and length in key structures of the prefrontal cortex necessary for cognitive, emotional, and behavioral control. Thus, emotional reactivity increases while the ability to regulate emotion simultaneously decreases. Behavioral genetic studies have demonstrated that genes affecting dopamine and serotonin transmission moderate the dose-response relationship between cumulative traumatic event exposure and PTSD vulnerability (Grabe et al., 2009
; Kolassa, Kolassa et al., 2010; Kolassa et al., in press; Xie et al., 2009
), and these same genes also affect emotion processing (Hariri et al., 2002
), cognitive flexibility (Krugel, Biele, Mohr, Li, & Heekeren, 2009
), and cognitive control of attention to threat (Beevers et al., 2007
; Bishop, Cohen, Fosella, Casey, & Farah, 2006
). This body of research implicates the key roles that cumulative traumatic event exposure and its neurobiological consequences play in the development of PTSD. From this perspective, it would be expected that individuals exposed to traumatic events, regardless of PTSD, would display disrupted attention towards threat. Further, a dose-response relationship between traumatic event exposure frequency and disrupted attentional control of threat would be expected. There is only limited evidence testing a relationship between trauma exposure frequency/severity and EST performance (McNally et al., 1990
). Future research along these lines will help clarify the source of impaired EST performance in PTSD, which will help clarify the dysfunctional processes characterizing PTSD.
If this interpretation were valid and these results do suggest that traumatic event exposure, regardless of PTSD, impairs attentional control and enhances threat processing, then the results are also inconsistent with the view that these processes are specifically linked with psychopathology. Instead, it may be the case that these processes are risk factors that confer vulnerability for psychopathology, or that they are correlated with some other processes that confer vulnerability for psychopathology. This may be consistent with research showing that 1) genes affecting serotonin transmission confer vulnerability to psychopathology following stressful events (Caspi et al., 2003
; Grabe et al., 2009
; Xie et al., 2009
), 2) these same genes modulate difficulty disengaging attention from threat among samples screened to be free from psychopathology (Beevers et al., 2009
), and 3) impaired performance in the EST has been found to predict distress to subsequent stressors (MacLeod & Hagan, 1992
). The fact that attentional biases towards threat are found in vulnerable, but psychopathology free, individuals is consistent with the view of these processes as risk factors for psychopathology instead of the view of these processes as markers of current psychopathology. One means of testing this conceptualization as it relates to PTSD specifically would be to measure prospectively EST performance, exposure to traumatic events, and symptoms of PTSD, which would allow for delineation of the temporal relationships between these processes.
In regards to the second purpose of the meta-analysis, the overall pattern of results provide support for hypoactive attentional control mechanisms in PTSD, but only weak support for a hyperactive threat detection mechanism in PTSD. When examining moderators of within-subjects effects, two key observations provide support for deficits in attentional control: 1) threat words only impaired performance in unmasked, but not masked, Stroop presentations, and 2) threat words impaired performance in blocked designs significantly more so than in randomized designs. The former effect demonstrates that performance impairment is only observed when some degree of elaborate and/or effortful processing is possible, which is consistent with the hypothesis of impaired attentional control. The latter effect demonstrates that the ‘slow’ (i.e., inter-trial) EST effect, which is dependent on attentional control (McKenna & Sharma, 2004
; Wyble et al., 2008
), is particularly pronounced among PTSD groups. Again, however, the larger effect in blocked designs may result from mood induction stemming from repeated presentations of threat words; thus, conclusions based solely on the block design manipulation must be tempered.
There were two key pieces of evidence for a hyperactive threat detection mechanism when examining within-subject comparisons. First, both PTSD-relevant and generally threatening words, but not positive words, significantly slowed RTs relative to neutral words among PTSD groups. Given that PTSD-relevant words may be more personally relevant for PTSD groups, performance disruptions from these words may not necessarily reflect threat processing. The finding that generally threatening words, but not positive words, also impair performance is consistent with the view that individuals with PTSD are more reactive to threat stimuli and not emotionality per se. Second, the EST effect size for PTSD-relevant and generally threatening words remained in the small range in randomized designs. As discussed above, randomized designs should reflect the ‘immediate’ (i.e., intra-trial) EST effect, hypothesized to be more dependent on emotional reactivity and less so on attentional control (Wyble and colleagues, 2008
); thus, meaningful effect sizes in these designs provides some support for enhanced threat detection. However, the key prediction from the hypothesis of enhanced threat detection was not supported: EST effect sizes in masked Stroop designs were generally of a trivial magnitude. Given that masking is a procedure commonly used to assess enhanced threat detection (Ohman & Soares, 1993
), the present failure to find strong evidence of an EST effect towards masked words notably tempers conclusions about enhanced threat detection in PTSD.
The only evidence from between-group comparisons for enhanced threat detection in PTSD is the fact that PTSD groups (and TC groups) differed from the NTC groups in attention towards threat above and beyond attention towards neutral stimuli. The fact that threat disrupted attentional performance above and beyond general attentional control impairment (i.e., longer reaction times towards threat words compared to neutral words) implicates some degree of enhanced threat processing. However, the fact that PTSD was not associated with greater EST effect sizes in masked or randomized designs is inconsistent with the enhanced threat detection hypothesis and qualifies strength of support for enhanced threat detection. The pattern of findings regarding hyperactive threat detection, then, suggests that enhanced threat detection may potentiate general attentional control deficits (i.e., an interacting system hypothesis). Enhanced threat detection may heighten prepotent responses towards threat stimuli (Williams et al., 1996
; Wyble et al., 2008
), which creates even greater demands on an already weakened attentional control system in PTSD. The key prediction from this hypothesis is that enhanced threat detection will only affect performance when attentional control demands are high and resources are low. By contrast, threat detection does not appear to be enhanced in PTSD to the degree that it impairs performance independent of attentional control functioning (i.e., does not facilitate detection of masked stimuli).
While the present data cannot directly speak to clinical implications, some tentative speculation might be warranted. There has been growing recent interest in attention training as an intervention for anxiety disorders, with preliminary reports suggesting significant reductions in anxiety symptoms (Amir et al., 2008Amir et al., 2009; Hazen et al., 2009; Schmidt et al., 2009). Attention training procedures generally present two stimuli, one threatening and one neutral, on a computer screen, and the participant’s task is to detect a subsequent probe that appears in a location previously occupied by either the threat or neutral stimulus. In the training condition, the probe appears most frequently in the location opposite to the threat stimuli; thus, participants are trained to disengage attention from threat stimuli. Indeed, the only study that has investigated which attentional bias components are affected by attention retraining (Amir et al., 2009) found improvements in disengagement from threat on a separate task. The current finding that enhanced threat processing disrupts attentional control in PTSD may implicate the need for such training procedures. Given that a sizeable percentage of PTSD patients receiving cognitive-behavioral treatments continue to exhibit significant symptoms post-treatment (Foa et al., 1991
; Schnurr et al., 2007
), it will be interesting to test whether adding attention retraining procedures can improve the efficacy of these treatments. Also, if impaired EST performance is indeed a risk factor for the subsequent development of PTSD, then attention retraining following traumatic event exposure regardless of PTSD could operate as a preventative intervention. Future research along these lines is necessary for both clinical and theoretical reasons.
It will also be important for future research to investigate how processes presumably measured by the EST (attentional control, threat detection) relate to the other mechanisms implicated in PTSD, such as memory dysfunction (Brewin et al., 2007
; McNally et al., 1995
), anxiety sensitivity (Marshall, Miles, & Stewart, 2010
), and emotion regulation difficulty (Tull et al., 2007
). The current conceptualization of these processes is that they represent relatively basic cognitive and emotional functions, which presumably makes them superordinate to some of the other processes implicated in PTSD (e.g., emotion regulation, anxiety sensitivity, avoidance). For example, given the developmental link between attentional control and self-regulation (Posner & Rothbart, 2000
), it might be expected that emotion regulation difficulties observed in PTSD are due to causally prior attentional control disruptions. Similarly, preoccupation with unpleasant interoceptive sensations could be due to enhanced detection of these danger signals and decreased ability to disengage attention from them. However, future research is clearly necessary to test this conceptualization. It will also be interesting to test how impaired attentional control and threat processing relate to memory dysfunction implicated in PTSD (Brewin et al., 2007
; McNally et al., 1995
). It could be the case that memory dysfunction and the current processes are either overlapping or distinct impairments. For example, perhaps overgeneral autobiographical memories (McNally et al., 1995
) and poor attentional control in the context of threat both reflect deficits in a shared higher-order cognitive control process. Future research is necessary to clarify the relationships between different cognitive dysfunctions identified in PTSD.
Several limitations must qualify conclusions from this study. First, the only mechanisms the current data address are those presumably measured by the EST. Discussion was accordingly focused on threat processing and attentional control, but it is important to note that the current results cannot speak to the relative centrality of attentional control and threat detection to understanding PTSD. Second, most of the studies using a blocked design also used a card format, as opposed to computerized format. This means that design is somewhat confounded with other experimental procedures and conclusions based on this manipulation must be tempered accordingly. Third, the EST is just one of many tasks used to assess attentional and emotional processes. It will be important for future research to continue to examine these processes using novel methodological approaches. Fourth, between-group differences were tested by comparing the within-group differences between the PTSD and comparison groups. This was done because of the significant group differences in performance on neutral trials, but this statistical approach is less powerful because the groups are not compared on a study by study basis, which would hold extraneous study factors (e.g., stimulus words, diagnostic procedures, data cleaning, etc.) constant. Fifth, it is uncommon for emotional words in EST research to be matched in arousal, and emerging research suggests that arousal, not valence, is more important for disrupting attentional processes (Anderson, 2005
). As such, it remains possible that any differences observed between emotional words (PTSD-threat versus general-threat versus positive) are due to differences in arousal and not due to valence or semantic category. While conclusions from this meta-analysis must accordingly be tempered, this meta-analysis represents the first attempt to quantitatively synthesize results from the EST research in PTSD and provides initial evidence for the negative consequences of trauma exposure on attention towards threat and for disrupted attentional control and enhanced threat detection.