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Cognitive inhibition in patients with medial orbitofrontal damage

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Abstract

Inhibition underlies cognitive processes such as overcoming habitual responses, suppressing of goal-irrelevant information, and switching of attention between stimuli or task rules. These processes are thought to depend on the frontal lobes. However, the precise role of the ventral frontal regions (orbitofrontal cortex) in these processes remains elusive. In the present study, our goal was to clarify the role of the orbitofrontal cortex in cognitive inhibition by examining the effects of focal lesions to the medial orbitofrontal cortex (posterior part of the gyrus rectus) on performance in tasks that required inhibitory control. Patients who had undergone surgery for an anterior communicating artery aneurysm and normal control subjects (C) participated in the study. The patients were subdivided into three groups: those with resection of the left (LGR+) or right (RGR+) gyrus rectus, and without such a resection (GR-). The Stroop Color-Word test, Trail Making B test, and the Category test were used as instruments for assessing response inhibition, switching between concrete stimuli, and switching between abstract task rules, respectively. In addition, the Digit Symbol test was used to examine sustained attention and processing speed. In the Stroop Color-Word test, the RGR+ group performed worse than all other groups. In the Trail Making B test, the RGR+ and LGR+ groups performed worse than both the GR- and C groups. In the Category test and Digit Symbol test, the groups did not differ significantly from each other. Our study indicates a specific contribution of the medial orbitofrontal cortex to response inhibition and stimulus-based switching of attention.

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Acknowledgements

This work was supported by grant 2 P05B 060 27 from the Polish Ministry of Scientific Research and Information Technology.

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Correspondence to Iwona Szatkowska.

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Szatkowska, I., Szymańska, O., Bojarski, P. et al. Cognitive inhibition in patients with medial orbitofrontal damage. Exp Brain Res 181, 109–115 (2007). https://doi.org/10.1007/s00221-007-0906-3

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