ABSTRACT
Hepatic encephalopathy (HE) is a neuropsychiatric disorder seen in patients with advanced liver disease or porto-systemic shunts. Based on etiology and severity of HE, the World Congress of Gastroenterology has divided HE into categories and sub-categories. Many user-friendly computer-based neuropsychiatric tests are being validated for diagnosing covert HE. Currently, emphasis is being given to view HE deficits as a continuous spectrum rather than distinct stages. Ammonia is believed to play crucial role in pathogenesis of HE via astrocyte swelling and cerebral edema. However, evidence has been building up which supports the synergistic role of oxidative stress, inflammation and neurosteroids in pathogenesis of HE. At present, treatment of HE aims at decreasing the production and intestinal absorption of ammonia. But as the role of new pathogenetic mechanisms becomes clear, many potential new treatment strategies may become available for clinician.
ABSTRACT
Until the advent of Liver transplantation, it was widely believed that Hepatic Encephalopathy (HE) was usually reversible. The exceptions were the so called "Acquired Hepatocerebral Degeneration cases" which were considered irreversible. Paradoxically, it seems, with liver transplantation, we have seen cases that contradict these rules. Whether the "residual effects" of HE, degenerative brain injury or independent neurological insults are causing post transplant neurological deficits is not easy to discern. As more emphasis is being put on maintaining brain 'status' after liver transplantation, we are finding confirmation of the largely reversible nature of HE. But, enough important exceptions to this rule are occurring to make further research on this topic mandatory.
