Early markers of neural dysfunction and compensation: A model from minimal hepatic encephalopathy

•Patients with MHE showed attention deficits, as revealed by the lower P3a and impaired performance.•Patients without MHE did not show a decline in performance, although they displayed a P3a reduction.•Patients without MHE showed an enhancement of the N2 and nogo-P3 amplitudes compared to controls.•The N2 and nogo-P3 increase reflects compensatory mechanisms recruited by patients without MHE.

ObjectiveThe 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.MethodsThe 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.ResultsPatients 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.ConclusionsBoth 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.SignificanceThe study suggests how initial brain dysfunction might be compensated for by recruitment of additional neurocognitive resources.