Giorgia Cona1, Sara Montagnese2, Patrizia Silvia Bisiacchi3, Angelo Gatta4, Umberto Cillo5, Paolo Angeli6, Piero Amodio7, Sami Schiff8. 1. Department of General Psychology, University of Padua, Via Venezia 8, 35131 Padua, Italy; CIRMANMEC, Via Giustiniani 2, 35128 Padua, Italy. Electronic address: giorgia.cona@unipd.it. 2. Department of Medicine, University of Padua, Via Giustiniani 2, 35128 Padua, Italy; CIRMANMEC, Via Giustiniani 2, 35128 Padua, Italy. Electronic address: sara.montagnese@unipd.it. 3. Department of General Psychology, University of Padua, Via Venezia 8, 35131 Padua, Italy; CIRMANMEC, Via Giustiniani 2, 35128 Padua, Italy. Electronic address: patrizia.bisiacchi@unipd.it. 4. Department of Medicine, University of Padua, Via Giustiniani 2, 35128 Padua, Italy; CIRMANMEC, Via Giustiniani 2, 35128 Padua, Italy. Electronic address: angelo.gatta@unipd.it. 5. Hepatobiliary Surgery, Department of Surgery, University of Padua, Via Giustiniani 2, 35128 Padua, Italy. Electronic address: cillo@unipd.it. 6. Department of Medicine, University of Padua, Via Giustiniani 2, 35128 Padua, Italy. Electronic address: pangeli@unipd.it. 7. Department of Medicine, University of Padua, Via Giustiniani 2, 35128 Padua, Italy; CIRMANMEC, Via Giustiniani 2, 35128 Padua, Italy. Electronic address: piero.amodio@unipd.it. 8. Department of Medicine, University of Padua, Via Giustiniani 2, 35128 Padua, Italy; CIRMANMEC, Via Giustiniani 2, 35128 Padua, Italy. Electronic address: sami.schiff@unipd.it.
Abstract
OBJECTIVE: The Inhibitory Control Task (ICT) was used to detect minimal hepatic encephalopathy (MHE). ICT assesses attention, working memory and inhibition by evaluating performance in detect, go and nogo trials, respectively. The event-related potentials (ERPs) elicited by the ICT provide insight into neural mechanisms underlying the cognitive alterations associated with MHE. METHODS: The performance and the ERPs elicited by ICT were measured in 31 patients with cirrhosis (13 with and 18 without MHE) and in 17 controls. The latency and amplitude of the N2, P3a, P3b and nogo-P3 were compared among the groups. RESULTS: Patients with MHE performed worse in all ICT trials compared to patients without MHE and controls. Cirrhotic patients, both with and without MHE, displayed a reduction in P3a amplitude, selectively in the detect trials. Patients without MHE exhibited greater N2 and nogo-P3 amplitudes compared to patients with MHE and controls. CONCLUSIONS: Both patients with and without MHE displayed neural alterations reflecting attentional deficits (i.e., P3a attenuation). However, patients without MHE coped with such dysfunctions by recruiting compensatory neural mechanisms, as suggested by the enhancement of the nogo-P3 and N2 amplitudes coupled with a normal ICT performance. SIGNIFICANCE: The study suggests how initial brain dysfunction might be compensated for by recruitment of additional neurocognitive resources.
OBJECTIVE: The Inhibitory Control Task (ICT) was used to detect minimal hepatic encephalopathy (MHE). ICT assesses attention, working memory and inhibition by evaluating performance in detect, go and nogo trials, respectively. The event-related potentials (ERPs) elicited by the ICT provide insight into neural mechanisms underlying the cognitive alterations associated with MHE. METHODS: The performance and the ERPs elicited by ICT were measured in 31 patients with cirrhosis (13 with and 18 without MHE) and in 17 controls. The latency and amplitude of the N2, P3a, P3b and nogo-P3 were compared among the groups. RESULTS:Patients with MHE performed worse in all ICT trials compared to patients without MHE and controls. Cirrhotic patients, both with and without MHE, displayed a reduction in P3a amplitude, selectively in the detect trials. Patients without MHE exhibited greater N2 and nogo-P3 amplitudes compared to patients with MHE and controls. CONCLUSIONS: Both patients with and without MHE displayed neural alterations reflecting attentional deficits (i.e., P3a attenuation). However, patients without MHE coped with such dysfunctions by recruiting compensatory neural mechanisms, as suggested by the enhancement of the nogo-P3 and N2 amplitudes coupled with a normal ICT performance. SIGNIFICANCE: The study suggests how initial brain dysfunction might be compensated for by recruitment of additional neurocognitive resources.
Authors: Marsha Y Morgan; Piero Amodio; Nicola A Cook; Clive D Jackson; Gerald Kircheis; Mette M Lauridsen; Sara Montagnese; Sami Schiff; Karin Weissenborn Journal: Metab Brain Dis Date: 2015-09-28 Impact factor: 3.584