肝性脑病的发病机理至今尚未完全清楚。虽然曾经提出过多种假说,但它们之中没有一种能解释全部的临床和生化特征。例如急性肝衰竭的肝性脑病,一般血氨不高,不能用氨中毒来解释。虽然假性神经介质说曾得到支持,认为左旋多巴在急性肝衰竭的肝性脑病中有清醒作用,然而动物实验却没有得到支持。应用大量章鱼胺注入鼠的脑室,足以使脑内大量去甲肾上腺素及多巴胺耗尽,但结果鼠的神志意识并没有改变。尽管输入支链氨基酸治疗门脉性脑病是一种普遍使用的疗法,但最近一些随机分配双盲对照研究的结果却认为无效。如Warren等 The pathogenesis of hepatic encephalopathy has not yet been fully understood. Although many hypotheses have been proposed, none of them can explain all of the clinical and biochemical characteristics. For example, acute hepatic failure hepatic encephalopathy, the general blood ammonia is not high, can not be explained by ammonia poisoning. Although pseudo-neurotransmitters have been said to support the belief that levodopa has a clear role in hepatic encephalopathy in acute liver failure, animal experiments have not been supported. Injection of large quantities of octopamine into the ventricles of rats is sufficient to deplete norepinephrine and dopamine in the brain but results in no change in the consciousness of the rats. Although the administration of branched-chain amino acids to portal vein encephalopathy is a commonly used therapy, the results of several randomized, double-blind, controlled studies are considered ineffective. Such as Warren and so on