Hepatic encephalopathy is associated with slowed and delayed stimulus-associated somatosensory alpha activity

•This study for the first time investigated alterations of oscillatory brain activity within the somatosensory system in hepatic encephalopathy (HE).•The frequency of somatosensory alpha activity was slowed and its stimulation-induced rebound delayed with increasing HE severity.•These findings provide further evidence for a global slowing of brain activity in HE and a deficit of somatosensory stimulus processing.

ObjectiveHepatic encephalopathy (HE) is associated with motor symptoms and attentional deficits, which are related to pathologically slowed oscillatory brain activity. Here, potential alterations of oscillatory activity in the somatosensory system were investigated.Methods21 patients with liver cirrhosis and varying HE severity and 7 control subjects received electrical stimulation of the right median nerve while brain activity was recorded using magnetoencephalography (MEG). Oscillatory activity within the contralateral primary somatosensory cortex (S1) and its stimulus-induced modulation were analyzed as a function of disease severity.ResultsMedian nerve stimuli evoked an early broadband power increase followed by suppression and then rebound of S1 alpha and beta activity. Increasing HE severity as quantified by the critical flicker frequency (CFF) was associated with a slowing of the alpha peak frequency and a delay of the alpha rebound.ConclusionThe present results provide the first evidence for a slowing of oscillatory activity in the somatosensory system in HE in combination with a previously unknown deficit of S1 in adjusting activation levels back to baseline.SignificanceThese findings advance the understanding of the manifold symptoms of HE by strengthening the theory that disease related slowing of oscillatory brain activity also affects the somatosensory system.