The basal ganglia and portal-systemic encephalopathy

Despite decades of research, the pathogenesis of portal-systemic encephalop athy (PSE) remains puzzling. Current hypotheses on the pathophysiology of P SE usually deal with metabolic toxins like ammonia or disturbances in neuro transmitter systems, especially glutamatergic or GABA-ergic neurotransmissi on. With respect to clinical, neuropathological, MRI and PET findings this review advances the hypothesis that the known alterations of neurotransmiss ion and astrocytic function in PSE might impair basal ganglia function in c irrhotics. The symptoms of PSE - whether cognitive, emotional or motor - ar e proposed to be a consequence of basal ganglia dysfunction.