PET and SPECT in Hepatic and Uraemic Encephalopathy

Abstract

Liver or kidney failure can disturb brain function to a variable extent. If organ failure is treated successfully, brain function is normally at least in part restored. A broad spectrum of radiotracer imaging methods has been employed to measure correlates of brain function and thereby elucidate the pathophysiology of hepatic or uraemic encephalopathy. Measurements of regional cerebral perfusion as well as energy metabolism in hepatic encephalopathy (HE) mostly revealed reductions in areas (particularly the frontal cortex and cingulum) relevant for the typically observed functional deficits (e.g. in attention or movement initiation). PET studies demonstrated that in HE, brain uptake of the neurotoxic ammonia increases with its plasma concentration. Some studies using the biomarker C-11-PK11195 indicate the presence of neuroinflammation in HE. Different neuroreceptor systems have been studied in HE throughout demonstrating reduced binding – particularly to central GABA-A receptors and dopamine as well as serotonin transporters. In patients with chronic renal failure and particularly those with depressive mood, reductions of cerebral blood flow and energy metabolism have been demonstrated, primarily located in the frontal cortex.