تعدیل استراتژی سرعت-دقت در افسردگی اساسی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|29824||2015||6 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Psychiatric Research, Volume 60, January 2015, Pages 103–108
Background Depression is associated with deficits in cognitive flexibility. The role of general slowing in modulating more specific cognitive deficits is however unclear. Aim We assessed how depression affects the capacity to strategically adapt behavior between harsh and prudent response modalities and how general and specific processes may contribute to performance deficits. Methods Patients suffering from major depression and age- and education-matched healthy controls were asked to randomly stress either speed or accuracy during perceptual decision-making. Results Diffusion models showed that patients with depression kept using a less conservative strategy after a trial with speed vs. accuracy instructions. Additionally, the depression group showed a slower rate of evidence accumulation as indicated by a generally lower drift rate. Conclusions These data demonstrate that less efficient strategic regulation of behavior in depression is due not only to general slowing, but also to more specific deficits, such as a rigid dependence on past contextual instructions. Future studies should investigate the neuro-anatomical basis of this deficit.
Depression is a major psychiatric disorder, which is usually accompanied by deficits in cognitive functioning, including impairments in cognitive flexibility (Airaksinen et al., 2004, Meiran et al., 2011 and Whitmer and Banich, 2007). In particular, Whitmer and Banich (2007), by using a task-switching paradigm, showed that depressive rumination is associated with deficits in inhibiting previous mental sets. Moreover, patients with major depression show significant deficits when performing the Wisconsin Card Sorting Test (WCST), a test of cognitive flexibility, including problems in shifting cognitive sets when appropriate (e.g., Franke et al., 1993 and Merriam et al., 1999). Perseverative responses and other deficits in the WCST are predicted by the severity of depressive symptoms independently of general intellectual abilities (Martin et al., 1991). Cognitive flexibility deficits are possibly mediated by prefrontal serotonin deficiency (Clarke et al., 2004). From the functional-anatomical point of view, the dorsolateral prefrontal cortex (especially on the left hemisphere), which is reliably activated during tasks tapping cognitive flexibility (Kim et al., 2011 and Vallesi, 2012), has been shown to be hypo-metabolic in depression (Bench et al., 1992, Davidson et al., 2002, Drevets, 2000 and Mayberg et al., 1999), although many fMRI studies have shown that this region may be inefficiently hyper-active during task execution (see Graham et al., 2013; for a recent meta-analysis). Depression is also accompanied by an abnormal pattern of activation of medial prefrontal structures such as the anterior cingulate cortex (Bench et al., 1992, Diener et al., 2012, Drevets et al., 1992 and Kennedy et al., 2001), a region implicated in energization, drive, and in the effortful allocation of cognitive and motor control (Paus, 2001, Shenhav et al., 2013, Stuss, 2011 and Vallesi, 2012). The prediction follows that patients suffering from major depression will show impairment in flexible regulation of behavior, especially in tasks recruiting the dorsolateral prefrontal cortex and the anterior cingulate cortex. Cognitive flexibility is for instance required when trading off speed and accuracy. This capacity is important in everyday life because it allows us to flexibly adapt to different and quickly changing environmental and endogenous demands. It has been shown that switching from speed to accuracy by adopting stricter criteria for decision-making involves the left dorsolateral prefrontal cortex (Vallesi et al., 2012). Patients suffering from depression are thus expected to be impaired in this condition. A second prediction concerns possible deficits in the energization process based on anterior cingulate cortex, which should produce generally slower responding (Stuss et al., 2005). Although a neuroimaging study should be set up to directly test the link between the involvement of these key regions and cognitive flexibility problems in depression, the present study aimed at finding behavioral evidence for deficits in speed-accuracy strategy regulations in major depression. A perceptual decision-making task was adopted in which speed and accuracy instructions were manipulated on a trial-by-trial basis to understand whether depression is associated with cognitive flexibility deficits in trials that require a switch in response strategy, and in slow response patterns especially in trial sequences with high time pressure. To gain deep insights on the possible mechanisms of depression-related deficits in speed-accuracy trade off regulation, we adopted a diffusion model analysis (e.g., Ratcliff, 1978 and Voss and Voss, 2007) of the performance data (i.e., response times and accuracy), which allowed us to estimate more informative decisional and non-decisional sub-processes.
نتیجه گیری انگلیسی
All the behavioral data are shown in Table 2. Table 2. Behavioral data shown according to group and task condition. For each variable, mean and standard error of the mean (S.E.M.) are shown. ‘Acc’ and ‘Spd’ stand for Accuracy and Speed current cues, respectively. ‘Prec Acc’ and ‘Prec Spd’ indicate accuracy and speed instructions in the preceding trial, respectively. Depression group Control group Prec Accuracy Prec speed Prec Accuracy Prec speed Acc Spd Acc Spd Acc Spd Acc Spd Accuracy (%) Training Phase Mean 83.8 83.0 84.0 84.5 90.7 90.6 91.3 89.9 S.E.M. 2.1 2.9 2.8 2.1 1.1 1.1 0.9 1.2 Test Phase Mean 94.0 89.5 89.2 86.8 93.1 91.9 93.8 93.1 S.E.M. 1.5 2.0 2.1 2.1 1.0 1.0 1.2 0.8 RTs (ms) Training Phase Mean 1051 972 1046 922 999 924 995 880 S.E.M. 30 48 32 41 39 32 39 33 Test Phase Mean 918 893 932 860 897 870 902 825 S.E.M. 37 43 34 40 34 34 37 36 Bias 'z/a' Training Phase Mean 0.58 0.57 0.52 0.56 0.52 0.54 0.52 0.57 S.E.M. 0.02 0.02 0.02 0.03 0.02 0.02 0.02 0.02 Test Phase Mean 0.58 0.58 0.54 0.56 0.56 0.58 0.57 0.61 S.E.M. 0.02 0.03 0.03 0.04 0.02 0.02 0.02 0.02 Distance 'a' Training Phase Mean 1.69 1.53 1.68 1.45 1.63 1.48 1.65 1.45 S.E.M. 0.06 0.05 0.06 0.06 0.04 0.05 0.05 0.04 Test Phase Mean 1.61 1.47 1.50 1.34 1.53 1.41 1.53 1.34 S.E.M. 0.07 0.07 0.06 0.07 0.05 0.05 0.05 0.05 Drift rate 'v' Training Phase Mean 0.96 1.10 1.23 1.30 1.72 1.73 1.75 1.70 S.E.M. 0.11 0.12 0.17 0.18 0.11 0.11 0.12 0.13 Test Phase Mean 2.06 1.69 1.64 1.81 2.28 1.87 2.02 2.08 S.E.M. 0.20 0.22 0.20 0.27 0.17 0.14 0.15 0.14 Table options Accuracy. In the ANOVA concerning the speed-accuracy experimental runs, there was a strong trend for a cue main effect [F(1, 46) = 3.73, p = .059], with participants being more accurate for accuracy (90%) than for speed cues (88.7%). Depressed patients were on average less accurate than their controls [86.8% vs. 91.8%; F(1, 46) = 10.13, p = .0026], although they were still able to perform the task with a reasonable accuracy level. Accuracy improved from the training phase with feedback (87.2%) to the test phase (91.4%) in both groups [F(1, 46) = 27.2, p < .0001]. An interaction between phase and group [F(1, 46) = 5.33, p = .025] was better qualified by a 3-way interaction with the preceding cue [F(1, 46) = 7.55, p = .008]. Post-hoc Tukey's tests revealed that this interaction was mainly due to differential sequential effects for the two groups in the test phase. Specifically, the accuracy level in the Depression group depended on the preceding cue type when no feedback was provided during the test phase, with worse accuracy when the current trial followed speed (88%) vs. accuracy (91.7%) instructions in the preceding trial (p = .004). There was no modulation by the preceding cue in the control group (93.4 vs. 92.5%; p = .97). This was further confirmed with separate ANOVAs for each phase, which revealed a significant preceding cue by group interaction for the test phase [F(1, 46) = 9.58, p = .0033], but not for the training one (p = .55). Correlation analyses performed on the depression group showed that, for the test phase, the difference between the two preceding cues (accuracy - speed) in terms of accuracy level was negatively correlated with the antidepressant rating scale (Spearman R = −0.52, p = .019), that is, the higher the antidepressant load, the smaller the differential carry-over effects from the preceding cue type. No other effect was significant. Response Times (RTs). RTs were shorter in the test run than in the training runs with feedback [887 vs. 974 ms; F(1, 46) = 40.57, p < .00001]. They were shorter for preceding speed cues than for preceding accuracy cues [920 vs. 940 ms; F(1, 46) = 13.25, p = .0007]. Moreover, RTs were shorter for current speed cues than accuracy cues [893 vs. 967 ms; F(1, 46) = 31.37, p < .00001], this difference being more accentuated in the training runs than in the test run [cue × phase interaction: F(1, 46) = 10.46, p = .002]. A preceding × current cue interaction [F(1, 46) = 27.3, p = .00001] was mainly due to the fact that RTs in speed trials preceded by speed trials were shorter than speed trials preceded by accuracy trials (872 vs. 915 ms, p = 0.0002), while the preceding cue did not modulate RTs for current accuracy trials (966 vs. 969 ms; p = .98). No other effect was significant.