Cognitive Inflexibility in Obsessive-Compulsive Disorder and Major Depression Is Associated with Distinct Neural Correlates

Abstract

Obsessive-compulsive disorder (OCD) and major depressive disorder (MDD) are frequently co-morbid, and dysfunctional frontal-striatal circuits have been implicated in both disorders. Neurobiological distinctions between OCD and MDD are insufficiently clear, and comparative neuroimaging studies are extremely scarce. OCD and MDD may be characterized by cognitive rigidity at the phenotype level, and frontal-striatal brain circuits constitute the neural substrate of intact cognitive flexibility. In the present study, 18 non-medicated MDD-free patients with OCD, 19 non-medicated OCD-free patients with MDD, and 29 matched healthy controls underwent functional magnetic resonance imaging during performance of a self-paced letter/digit task switching paradigm. Results showed that both patient groups responded slower relative to controls during repeat events, but only in OCD patients slowing was associated with decreased error rates. During switching, patients with OCD showed increased activation of the putamen, anterior cingulate and insula, whereas MDD patients recruited inferior parietal cortex and precuneus to a lesser extent. Patients with OCD and MDD commonly failed to reveal anterior prefrontal cortex activation during switching. This study shows subtle behavioral abnormalities on a measure of cognitive flexibility in MDD and OCD, associated with differential frontal-striatal brain dysfunction in both disorders. These findings may add to the development of biological markers that more precisely characterize frequently co-morbid neuropsychiatric disorders such as OCD and MDD.

Cognitive control interventions for depression: A systematic review of findings from training studies

“…Interestingly, the research shows that the engagement with training is key to obtain transfer effects in interaction with the levels of cognitive impairment at the onset of training. This suggests that not everyone with depression risk or complaints will benefit from training because (a) their working memory functioning is not impaired (for instance, Owens et al, 2012 showed individuals with high depression levels frequently have intact working memory capacity); and (b) they are insufficiently able to engage in training because of several reasons (e.g., lack of motivation). Clinically, we may need to apply CCT in a more tailored intervention based on participant status and working memory baseline measures.…”

“…There is extensive research showing that multiple cognitive biases at the level of attention, interpretation and memory influence depressive symptoms through their influence on stress reactivity (for reviews, see Everaert, Koster, & Derakshan, 2012;Farb, Irving, Anderson, & Segal, 2015;Gotlib & Joormann, 2010). Interestingly, recent work has shown that cognitive control over emotional information is linked to a host of these information-processing biases (Everaert, Grahek, & Koster, 2016), where the specific interplay between such biases has also been linked to rumination and depressive symptoms (Everaert, Grahek, Van den Bergh, et al, 2016).…”

“…For instance, cognitive control deficits have been observed in participants showing heightened trait rumination (e.g., Beckwé, Deroost, Koster, De Lissnyder, & De Raedt, 2014) and subclinical levels of depressive symptomatology (dysphorics; e.g., Derakshan, Salt, & Koster, 2009;Joormann, 2004;Owens, Koster, & Derakshan, 2012). Similarly, cognitive control impairments have been observed in a vast amount of studies exploring cognitive functioning in depressive patients (e.g., Deveney & Deldin, 2006;Goeleven, De Raedt, Baert, & Koster, 2006;Harvey et al, 2004;Levens & Gotlib, 2010;Merriam, Thase, Haas, Keshavan, & Sweeney, 1999;Murphy et al, 1999), and remain evident following remission from depression (e.g., Demeyer, De Lissnyder, Koster, & De Raedt, 2012;Levens & Gotlib, 2015;Paelecke-Habermann, Pohl, & Leplow, 2005;Vanderhasselt & De Raedt, 2009).…”

Meta-analytic investigations of structural grey matter, executive domain-related functional activations, and white matter diffusivity in obsessive compulsive disorder: An integrative review

“…Of the 35 articles, 19 articles employed executive function tasks and contributed studies for inclusion in the three themes: 6 studies in Theme 1 (Response Inhibition), 11 studies in Theme 2 (Interference) and 6 studies in Theme 3 (Set-shifting/switching) (Britton et al, 2010;de Wit et al, 2012b;Fitzgerald et al, 2005Fitzgerald et al, , 2010Gu et al, 2008;Han et al, 2011;Huyser et al, 2011;Kang et al, 2013;Maltby et al, 2005;Marsh et al, 2013;Nabeyama et al, 2008;Nakao et al, 2005Nakao et al, , 2009Page et al, 2009;Remijnse et al, 2013;Roth et al, 2007;Schlosser et al, 2010;Woolley et al, 2008;Yucel et al, 2007). Notably, 2 articles employed multiple tasks and contributed studies in all three themes (Page et al, 2009;Woolley et al, 2008).…”

“…Theme 3: 'Switching and Shifting' included 5 articles (4 on adults, 1 on adolescents) that adopted switching and shifting paradigms, contributing a total of 54 foci (52 from adults, 2 from adolescents), of which 3 foci (from a single study) (Remijnse et al, 2013) corresponded to increased activations and 51 foci (46 from adults, 5 from adolescents) corresponded to reduced activations in a total of 55 adult and 10 adolescent patients with OCD compared to 61 adult and 9 adolescent controls. Separate metaanalyses were conducted in accordance to their individual themes.…”