The basal ganglia and portal-systemic encephalopathy

Abstract

Despite decades of research, the pathogenesis of portal-systemic encephalopathy (PSE) remains puzzling. Current hypotheses on the pathophysiology of PSE usually deal with metabolic toxins like ammonia or disturbances in neurotransmitter systems, especially glutamatergic or GABA-ergic neurotransmission. With respect to clinical, neuropathological, MRI and PET findings this review advances the hypothesis that the known alterations of neurotransmission and astrocytic function in PSE might impair basal ganglia function in cirrhotics. The symptoms of PSE - whether cognitive, emotional or motor - are proposed to be a consequence of basal ganglia dysfunction.