Hindawi Publishing Corporation Epilepsy Research and Treatment Volume 2011, Article ID 596174, 11 pages doi:10.1155/2011/596174 Research Article Executive Functions in Chronic Mesial Temporal Lobe Epilepsy Laura Zamarian, 1 Eugen Trinka, 1, 2 Elisabeth Bonatti, 1 Giorgi Kuchukhidze, 1 Thomas Bodner, 1 Thomas Benke, 1 Florian Koppelstaetter, 3 and Margarete Delazer 1 1 Clinical Department of Neurology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria 2 Department of Neurology, Christian Doppler Clinic, Paracelsus Medical University, Ignaz Herrer Strasse 79, 5020 Salzburg, Austria 3 Clinical Department of Radiology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria Correspondence should be addressed to Laura Zamarian, laura.zamarian@uki.at Received 24 August 2010; Revised 6 December 2010; Accepted 11 January 2011 Academic Editor: Andreas Schulze-Bonhage Copyright © 2011 Laura Zamarian et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. There is no consensus as to whether mesial temporal lobe epilepsy (MTLE) leads to executive function deficits. In this study, we adopted an extensive neuropsychological test battery and assessed different executive functions in chronic, unilateral MTLE. Performance of MTLE patients was compared with that of healthy peers and with normative data. Several MTLE patients had scores below cut-off or below the 10th percentile of normative data. Scores of the whole patient group were overall in the average range of normative data. Relative to controls, MTLE patients performed poorly in tests of working memory, cognitive flexibility, categorical verbal fluency, set-shifting, categorization, and planning. These findings raise an important methodological issue as they suggest that executive function deficits in chronic MTLE may be individually variable and that their assessment should include different tests. Deficits in chronic MTLE are not limited to temporal lobe functions, such as memory, but may extend to extra temporal cognitive domains, such as executive functions. 1. Introduction Mesial temporal lobe epilepsy (MTLE) is possibly the most frequent form of epilepsy [1] and is associated with overt or subtle structural abnormalities in the hippocam- pus, parahippocampal gyrus, and amygdala [2]. Recent investigations have suggested that functional and structural abnormalities in MTLE may extend beyond the temporal lobes. Volume reduction has been observed in extratemporal areas such as thalamus, caudate nuclei, lenticular nuclei, corpus callosum, and frontal lobes (for a review, see [3]). Alterations of frontotemporal white matter tracts [4] and of neurotransmitter systems [5] have also been reported. Metabolic changes have been observed not only in mesial and lateral temporal areas, but also in the prefrontal cortex [6] and in subcortical structures [7, 8]. Thalamus, basal ganglia, and frontal lobes are part of corticosubcortical circuits that are involved in the regulation of motor functions, behavior, and cognitive functions such as set-shifting, planning, and inhibitory control [9, 10]. As increasing evidence points to functional and structural alterations of these corticosub- cortical circuits, it may be expected that MTLE patients experience executive function deficits. The term “executive functions” refers to high-order cog- nitive functions which allow adaptation to nonroutine sit- uations such as novel, conflicting, or complex tasks [11, 12]. Planning, set-shifting, strategic behavior, response initiation, and response inhibition are some of the cognitive functions that may be listed under this umbrella term. Executive function deficits are often found in association with frontal lobe damage [13, 14]. However, recent neuropsychological investigations as well as neuroimaging studies have pointed to a distributed brain network, which encompasses frontal areas as well as posterior areas (e.g., parietal association areas: [15]; cerebellum: [16]) and subcortical structures (e.g., basal ganglia: [17]; thalamus: [18]). Executive function deficits may be found in a large number of neurological pathologies, in diffuse brain damage, and in focal brain damage [11, 12]. Single-case analyses of brain-damaged patients have shown that executive function deficits may have different