Hepatic myelopathy, also known as portal-cavernous shunt myelopathy, is a specific type of neurological complication of liver disease, characterized by slowly progressive spastic paraplegia and predominantly demyelinating pathological changes in the lateral and posterior cords of the spinal cord. It occurs most often in the decompensated phase of cirrhosis, with prominent manifestations of hepatic decompensation and portal hypertension. Most patients have recurrent upper gastrointestinal bleeding, after portal-body vein shunts and splenorenal vein anastomoses. Most cases are seen with surgery or naturally formed portacaval circulation shunts. Most cases coexist with hepatic encephalopathy, and often spinal cord symptoms are masked by the consciousness and motor deficits of severe encephalopathy and no diagnosis can be made until demyelinating changes in the posterior and lateral spinal cords are detected on pathological examination. In those without a history of surgery, there is often significant abdominal wall varices, suggesting that a portal-body venous shunt has formed naturally. The disease occurs most often in the decompensated phase of cirrhosis, with prominent manifestations of hepatic decompensation and portal hypertension. Most patients have recurrent upper gastrointestinal bleeding, portal-body static venous shunts, and splenorenal venous anastomosis after hepatic myelopathy. Those without a surgical history often have significant abdominal wall varices, suggesting that a portal-body venous shunt has developed naturally. The etiology and pathogenesis are mainly related to 3 factors: severe cirrhosis; presence of abundant portal blood shunts (including surgical shunts or extensive collateral circulation); and chronic hyperammonia. It may also be associated with a variety of factors such as impaired protein metabolism, malnutrition, vitamin B deficiency and accumulation of toxic metabolites in the body. Usually half of hepatic myelopathy is caused by portal hepatic sclerosis and 1/3 is due to viral hepatitis. It is generally believed that it may be related to liver detoxification dysfunction and brain tissue metabolic disorders caused by increased blood ammonia. In addition, it is related to the formation of pseudo-mediators similar in structure to catecholamines during protein metabolism, which interferes with the normal transmission of mediators of the brainstem reticular activation system. Hepatic myelopathy is most often seen in patients with multiple episodes of hepatic encephalopathy who have undergone portal shunts and partial gastrectomy. The principles of treatment are to protect the liver, lower the blood ammonia and promote the recovery of spinal cord function. Because of the complex pathogenesis and multifactorial involvement, comprehensive measures are needed. 1, reduce the production and absorption of intestinal toxins hepatic myelopathy (1) diet and nutrition: limit the intake of protein, supply calories 5.0-6.7kPa and sufficient vitamins every day, with sugar as the main food, and then gradually increase to the patient can tolerate according to clinical symptoms and blood ammonia measurement. Vegetable protein is the best. Vegetable protein contains less methionine and aromatic amino acids and more branched chain amino acids, and it can increase fecal nitrogen excretion. In addition, vegetable protein contains non-absorbable fibers, which are fermented by the intestines to produce acid to facilitate the elimination of ammonia, and is conducive to laxation. (2) enema or diarrhea: remove the intestinal accumulation of food, blood or other nitrogenous substances, saline or weak acidic solution (such as dilute acetic acid solution) enema, or oral or nasal feeding 33% magnesium sulfate 30 ~ 60ml diarrhea. Lactulose (lactulose) orally or by enema as the first choice. Lactulose is decomposed into lactic acid and acetic acid by bacteria in the colon after oral administration, making the intestinal lumen acidic, thus reducing the formation and absorption of ammonia, while promoting the growth of beneficial bacteria. (3) Inhibit bacterial growth: oral neomycin 2~4g/d or optional desmethylvancomycin are effective. 2.Promote the metabolic clearance of toxic substances and correct amino acid metabolic disorders. (1) Ammonia-lowering treatment: potassium/sodium glutamate, arginine, sodium benzoate, phenylacetic acid, ornithine – ketoglutarate and ornithine, and menthol has significant ammonia-lowering effect. (2) Branched-chain amino acids: oral or intravenous injection of amino acid mixture based on branched-chain amino acids can theoretically correct the imbalance of amino acid metabolism and inhibit the formation of pseudoneurotransmitters in the brain, but the efficacy in portal-somatic shunt encephalopathy is controversial. For those who cannot tolerate protein food, intake of sufficient amount of mixture rich in branched-chain amino acids is effective and safe for restoring positive nitrogen balance of patients. (3) Artificial liver: Hemoperfusion with activated charcoal and resin or hemodialysis with polyacrylonitrile can remove blood ammonia and other toxic substances. (3) Treatment of spinal cord disease intrathecal injection of dexamethasone can stop the demyelination of the spinal cord cone bundle, and the recent efficacy is still possible. On the basis of liver preservation, acupuncture, physiotherapy, massage and Chinese herbal medicine also have different degrees of improvement. 4, liver transplantation liver transplantation is an effective treatment for various end-stage liver diseases, and various stubborn and serious complications can be significantly improved after transplantation.