Abstract
Growing empirical evidence suggests that cognitive and affective problems in depression may be a reflection of cognitive control impairments. However, to date, the nature of such impairments is still poorly understood and further investigation of this topic is required to advance current knowledge on the underlying vulnerability factors for depression. Using a mixed antisaccade paradigm, the present study examined if depressive symptoms in general, and more specifically rumination, are related to impairments in cognitive control functions such as inhibition and switching. The results on antisaccade latency and error rates indicated that depressive symptoms in general were not related to impairments in inhibition and switching. However, rumination was associated with impaired inhibition such that high, compared to low, ruminators had slower antisaccade latencies. No group differences were observed on antisaccade error rates. Implications for understanding the underlying vulnerability factors for the development of depressive symptoms are discussed.
Acknowledgements
This work was supported in part by a Royal Society International Joint Project Grant awarded to Nazanin Derakshan and Ernst H. W. Koster. The research was carried out by Evi De Lissnyder, under the supervision of Naz Derakshan and Ernst H. W. Koster, at the Affective and Cognitive Neuroscience Lab at Birkbeck University of London. The authors declare no conflicts of interest. The first author, Evi De Lissnyder, is funded as a Research Assistant of the Fund for Scientific Research-Flanders (FWO), Belgium.
The authors would like to thank Tahereh L. Ansari and Dr Leor Shoker for help with programming and data preparation.
Notes
1This distractor task consists of blotting out the letters E and F on a paper covered with letters and took only five minutes. This task was administered to prevent potential emotional responses to performance difficulties on the antisaccade task (as hypothesised) from influencing the questionnaires.
2Switching can also be examined within the mixed block by performing a trial-by-trial analysis by comparing switch (trials preceded by a different trial type) to repeat (trials preceded by the same trial type) trials (Ansari et al., 2008). The analysis within the mixed block revealed the same results as the single to mixed block comparisons but due to length considerations these analyses were not included in this manuscript.