Changes in brain metabolism in hepatic encephalopathy.
Changes in brain metabolism in hepatic encephalopathy.
复制标题
肝性脑病脑代谢的变化。
DOI：
10.1007/bf02833600
复制
发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Biebuyck,JF
中科院分区：
文献类型：
--
作者：
Hawkins,RA;Mans,AM;Biebuyck,JF
Hepatic encephalopathy in patients may result from the surgical formation of a portacaval shunt or chronic liver disease, often accompanied by portal systemic shunting (Hoyumpa et al., 1979; Zieve, 1979; Misra, 1981). Whether the development of encephalopathy is caused by diversion of blood past the liver, decreased liver function, or both, is open to question. There is general agreement that the brain becomes much more sensitive to a variety of metabolic disturbances, that in normal individuals would cause no serious alterations in cerebral function. A gradient of symptoms ranging from subtle alterations in consciousness and mental ability to disorientation, stupor, and coma can be produced by increased dietary protein, gastrointestinal bleeding, infection, sedatives, or hyperammonemia. The apparent reversibility of these symptoms suggests that the encephalopathy has a metabolic etiology. Hepatic encephalopathy is a continuum of mentally deranged states. It is important to realize that encephalopathy may exist even when clinical symptoms are not obvious. Close studies of patients with liver disease show that psychomotor defects are present that are not apparent to the casual observer (Rehnstrom et al., 1977; Zieve, 1979). Cerebral oxidative me-
