اختلال چشمک زدن توجه در اختلال اضطراب اجتماعی: افسردگی مسائل همبودی

Abstract Background and objectives Difficulties with attentional control have long been thought to play a key role in anxiety and depressive disorders. However, the nature and extent of attentional control difficulties in social anxiety disorder (SAD) are not yet well understood. The current study was designed to assess whether attentional control for non-emotional information is impaired in SAD when taking comorbid depression into account.. Methods Individuals with SAD and healthy controls (HCs) were administered an attentional blink (AB) task in which they identified number targets in a rapid serial visual presentation stream of letters. Results Individuals with SAD and current comorbid depression exhibited reduced accuracy to identify a target that fell within the AB window after the presentation of a first target compared to individuals with SAD without current comorbid depression, as well as to HCs. The latter two groups did not differ from each other, and the three groups did not differ in accuracy for the second target when it was presented after the AB window. Limitations Although we included two clinical groups and the sample size for the non-comorbid SAD group was large, the comorbid SAD group was relatively small. Conclusions These results suggest that impaired attentional control among individuals with SAD may be limited to those suffering from current comorbid depression..

Introduction One mechanism thought to underlie social anxiety disorder (SAD) is attentional dyscontrol. In particular, heightened self-focused attention accompanied by undue capture of attention by social threat-relevant information in the environment is thought to contribute to difficulties maintaining attention on task-relevant goals in social situations (Clark and Wells, 1995 and Heimberg et al., 2014). Moreover, post-event processing, or the ruminative review of one's actions and the reactions of others that occurs between social situations and that is typical of persons with SAD (Brozovich & Heimberg, 2008), has the potential to perpetuate attentional dyscontrol even outside of the context of social situations. Attentional control theory (Eysenck and Derakshan, 2011 and Eysenck et al., 2007) provides a useful framework for conceptualizing attentional processing in SAD. Attentional control theory posits that high levels of anxiety impair the goal-directed attentional system (i.e., attentional control) by increasing the influence of the stimulus-driven attentional system. This imbalance results in biased attention toward salient stimuli, typically defined in terms of central location in the visual field, but also in terms of threat relevance. Highly anxious individuals are purported to have difficulties inhibiting and shifting attention away from task-irrelevant stimuli, especially when such stimuli are threat-relevant (Eysenck et al., 2007). In light of the suggestion that attentional dyscontrol in SAD may extend into the relative calm that separates anxiety-provoking experiences, it is plausible that difficulties with attentional control may occur not only in the context of task-irrelevant threat distractors, but also in the context of neutral distracting information. Whereas there are many studies on the former hypothesis, albeit with sometimes inconsistent results, far less is known about the latter hypothesis. If the broader tenets of attentional control theory extend to SAD, this could illuminate a potential transdiagnostic mechanism involved in the maintenance of anxiety disorders. In what follows, we review the literatures on attentional control in the context of 1) emotional task-irrelevant (threat) distractors and 2) non-emotional task-irrelevant (neutral) distractors, attempting to unify the findings under the framework of attentional control theory. Evidence of attentional dyscontrol in SAD in the context of emotional task-irrelevant stimuli comes primarily from studies of attention bias to threat. Meta-analytic results on the dot-probe task, spatial cuing task, and emotional Stroop task indicate a moderate between-group effect size of attention bias to threat in individuals with SAD compared to non-anxious individuals (d = .46; Bar-Haim, Lamy, Pergamin, Bakermans-Kranenburg, & van IJzendoorn, 2007). Biases toward threat in individuals with SAD or elevated social anxiety have also been reported in various other paradigms, such as the emotional antisaccade task ( Wieser, Pauli, & Mühlberger, 2009), emotional attentional blink task (for review see Van Bockstaele et al., 2014), and eye-tracking studies (e.g., Gamble & Rapee, 2010). Consistent with attentional control theory, observed biases have been attributed to biased engagement of attention with threat (enhanced stimulus-driven attention), difficulties disengaging attention from threat (impaired shifting away from threat), or both (e.g., Clarke, MacLeod, & Guastella, 2013). Nevertheless, studies on attention bias to threat in SAD are not equivocal, with several studies reporting null results (e.g., Heeren, Mogoaşe, McNally, Schmitz, & Philippot, 2015) or attention biases away from threat (see Bögels & Mansell, 2004). These discrepancies are important, as they suggest the possibility of moderators of attention bias to threat. One likely moderator that is often neglected is depression comorbidity ( Bar-Haim et al., 2007). Approximately 40–50% of individuals with a principal diagnosis of SAD also have major depressive disorder (MDD) or dysthymic disorder ( Brown, Campbell, Lehman, Grisham, & Mancill, 2001), and depression has been associated with broad impairments in executive functioning (for a review, see Snyder, 2013). Indeed, attention bias toward threat in individuals with elevated social anxiety was nullified, or at least dampened, in those with comorbid depression ( Grant and Beck, 2006, LeMoult and Joormann, 2012 and Musa et al., 2003). In contrast to the vast attention bias literature, no study to date has examined whether attentional control in the context of neutral task-irrelevant stimuli in SAD is impaired. Three studies in undergraduate samples suggest this may be the case. In two studies, self-reported attentional control was negatively correlated with social anxiety, even after statistically controlling for the effects of depression (Moriya and Tanno, 2008 and Morrison and Heimberg, 2013). In a third study, social anxiety was positively correlated with difficulty disengaging attention from non-emotional, task-irrelevant stimuli being held in working memory (Moriya & Sugiura, 2012). However, this effect was not moderated by working memory load. In theory, higher working memory load should be associated with a stronger association between anxiety and inhibitory difficulties, as attentional control resources are more consumed. Taken together, there is preliminary evidence of general attentional control difficulties in individuals with elevated social anxiety, but this research has been mostly limited to self-report studies, and the effects of depressive symptoms has only been considered through analyses of covariance, which may be inappropriate in this context (Miller & Chapman, 2001).1 To further our understanding of attentional dyscontrol in SAD, we sought to address the question of whether attentional control in the context of non-emotional stimuli is impaired in individuals with SAD, while also accounting for the often neglected and likely moderating effects of comorbid depression. Further, given criticisms of the psychometric properties of attention bias tasks often used in the anxiety disorders (e.g., Schmukle, 2005), we sought to use a well-established measure of attentional control, namely, the attentional blink (AB) task (see Martens & Wyble, 2010). The AB refers to the robust finding that accuracy to identify a second target (T2) following a first target (T1) in a rapid serial visual presentation (RSVP) stream of non-targets is relatively reduced when the lag between T1 and T2 is short (200–500 ms) compared to when it is long (over 500 ms). The reduced accuracy for short-delay T2 is thought to result from a temporary loss of attentional control (Di Lollo, Kawahara, Ghorashi, & Enns, 2005). In the current study, we examined AB performance in non-anxious, non-depressed healthy control participants (HCs) and in individuals with generalized SAD, either with or without current comorbid depression (MDD or dysthymic disorder). We hypothesized that, compared to HCs, individuals with SAD would (a) exhibit impaired attentional control (i.e., reduced accuracy for T2 presented within the AB window compared to a baseline condition) and (b) this relative impairment would be greatest for those with current comorbid depression.

Results 3.1. Preliminary analyses Demographic and clinical characteristics of participants are presented in Table 1. The three groups did not differ significantly in sex distribution, χ2(2, N = 203) = 3.61, p = .17, V = .09; age, F(2, 200) = .37, p = .69, View the MathML sourceηp2 = .004; years of education, F(2, 194) = 1.38, p = .26, View the MathML sourceηp2 = .01; or race/ethnicity composition (i.e., white versus non-white), χ2(2, N = 187) = 2.32, p = .31, V = .08. As expected, the groups differed significantly in their depression scores, F(2, 183) = 37.53, p < .001, View the MathML sourceηp2 = .29; the COM group had the highest BDI-II scores, followed by the SAD group, followed by the HC group, ps < .005. As expected, the groups differed significantly in their social anxiety scores, F(2, 196) = 313.27, p < .001, View the MathML sourceηp2 = .76; the HC group had significantly lower LSAS-SR scores than the SAD and COM groups, ps < .001, whose scores did not differ from each other, t(160) = 1.03, p = .31, d = .16. Table 1. Participant characteristics by diagnostic group. HC (n = 37) SAD (n = 140) COM (n = 26) Age, years (SD) 32.1 (8.6) 32.8 (8.2) 33.9 (7.8) Education, years (SD) 17.4 (2.8) 16.7 (2.5) 16.4 (2.4) Sex (% female) 59.5 57.9 38.5 % Race/ethnicity Asian-American 33 41 31 Black/African-American 0 1 0 Hispanic/Latino 8 7 11 White/Caucasian 51 43 54 Other 8 8 4 LSAS-SR 14.2 (9.5) 89.0 (18.0) 93.0 (16.5) BDI-II 1.5 (2.6) 10.0 (9.4) 21.4 (9.2) Note: HC = healthy control group; SAD = social anxiety disorder and no current depression group; COM = social anxiety disorder and comorbid depression group; LSAS-SR = Liebowitz Social Anxiety Scale, Self-Report Version; BDI-II = Beck Depression Inventory, 2nd Edition. Standard deviations in parentheses. Table options 3.2. AB effect An AB effect is reflected by contrasting short-lag T2|T1 accuracy with accuracy for a baseline condition (MacLean & Arnell, 2012). Most often, long-lag T2|T1 accuracy is used as the baseline; however, MacLean and Arnell (2012) explain that this baseline may underestimate the AB effect, particularly in samples with perceptual or cognitive impairment (e.g., Husain, Shapiro, Martin, & Kennard, 1997). Given findings of impaired executive functioning in depression, we used an additional baseline suggested by MacLean and Arnell (2012), that is, T1 accuracy. A 3 group (COM, SAD, HC) X 3 target (short-delay T2|T1, long-delay T2|T1, T1) mixed model Analysis of Variance (ANOVA) on percent accuracy revealed a significant main effect of group, F(2, 200) = 4.89, p < .01, View the MathML sourceηp2 = .05, and a significant main effect of target, F (2, 400) = 323.52, p < .001, View the MathML sourceηp2 = .62. The signature AB effect is lower accuracy for short-delay T2|T1 relative to the baseline, which was true for all three groups relative to both long-delay T2|T1 as baseline [HC t(36) = 5.71, p < .001, d = .94; SAD t(139) = 16.89, p < .001, d = 1.43; COM t(25) = 9.70, p < .001, d = 1.90] and relative to T1 as baseline [HC t(36) = 8.71, p < .001, d = 1.43; SAD t(139) = 25.27, p < .001, d = 2.14; COM t(25) = 16.00, p < .001, d = 3.14]. See Table 2 for mean accuracy rates for each of the three target types by group. Table 2. Mean percentage of accurate identifications of targets by target type and group. HC SAD COM Short-delay T2|T1 44.9 (27.3) 36.9 (23.2) 23.3 (19.9) Long-delay T2|T1 72.6 (25.7) 70.7 (17.9) 64.8 (25.3) T1 84.2 (12.2) 82.8 (10.7) 78.4 (13.6) Note: HC = healthy control group; SAD = social anxiety disorder and no current depression group; COM = social anxiety disorder and comorbid depression group; T1 = first target in rapid serial visual presentation stream; T2 = second target. Standard deviations in parentheses. Table options The predicted interaction of group × target was also significant, F(4, 400) = 2.52, p = .04, View the MathML sourceηp2 = .025. See Fig. 1. Follow-up tests contrasting short-delay T2|T1 accuracy to each of the baselines were first conducted. A 3 group × 2 target (short-delay T2|T1, long-delay T2|T1) ANOVA revealed an interaction that did not quite reach significance, F(2, 200) = 2.41, p = .09, View the MathML sourceηp2 = .02, whereas a 3 group × 2 target (short-delay T2|T1, T1) ANOVA yielded a significant interaction, F(2, 200) = 3.87, p = .02, View the MathML sourceηp2 = .04. Follow-up tests comparing groups on each of the three targets was then conducted. A one-way ANOVA comparing the three groups' accuracy for short-delay T2|T1 was significant, F(2, 200) = 6.42, p = .002, View the MathML sourceηp2 = .06. The COM group was significantly less accurate than the other two groups (vs. HC: t(61) = 3.44, p = .001, d = .88; vs. SAD: t(164) = 2.80, p = .006, d = .44). In contrast, the SAD group did not differ from the HCs, t(175) = 1.79, p = .08, d = .27. Because the SAD and COM groups did not differ on the LSAS-SR, it is unlikely that the relatively poorer performance of the COM group was due to greater social anxiety. No significant group differences were found for either of the baseline conditions [long-delay T2|T1: F(2, 200) = 1.19, p = .31, View the MathML sourceηp2 = .01; T1: F(2, 200) = 2.13, p = .12, View the MathML sourceηp2 = .02], indicating that group differences in processing of targets was limited to targets occurring within the AB window. Mean percentage of accurate T2|T1 responses for short-delay (336 ms) dual-target ... Fig. 1. Mean percentage of accurate T2|T1 responses for short-delay (336 ms) dual-target trials, T2|T1 responses for long-delay (672 ms) dual-target trials, and T1 responses in healthy control (HC) participants, participants with SAD without comorbid depression (SAD), and participants with SAD with comorbid depression (COM). Error bars are standard errors.