A neural mass model for disturbance of alpha rhythm in the minimal hepatic encephalopathy

Abstract

One of the early markers of minimal hepatic encephalopathy (MHE) is the disruption of alpha rhythm observed in electroencephalogram (EEG) signals. However, the underlying mechanisms responsible for this occurrence remain poorly understood. To address this gap, we develop a novel biophysical model MHE-AWD-NCM, encompassing the communication dynamics between a cortical neuron population (CNP) and an astrocyte population (AP), aimed at investigating the relationship between alpha wave disturbance (AWD) and mechanistical principles, specifically concerning astrocyte-neuronal communication in the context of MHE. In addition, we introduce the concepts of peak power density and peak frequency within the alpha band as quantitative measures of AWD. Our model faithfully reproduces the characteristic EEG phenomenology during MHE and shows how impairments of communication between CNP and AP could promote AWD. The results suggest that the disruptions in feedback neurotransmission from AP to CNP, along with the inhibition of GABA uptake by AP from the extracellular space, contribute to the observed AWD. Moreover, we found that the variation of external excitatory stimuli on CNP may play a key role in AWD in MHE. Finally, the sensitivity analysis is also performed to assess the relative significance of above factors in influencing AWD. Our findings align with the physiological observations and provide a more comprehensive understanding of the complex interplay of astrocyte-neuronal communication that underlies the AWD observed in MHE, which potentially may help to explore the targeted therapeutic interventions for the early stage of hepatic encephalopathy.