I. What is hepatic myelopathy? Hepatic myelopathy is a kind of cirrhotic portal hypertension developed to a certain degree, due to the naturally occurring extensive portal vein collateral circulation or portal vein shunt surgery after the emergence of the syndrome, with spinal cord lesions as the main symptom. Previously, due to the late start of the recognition of this disease and the lack of knowledge of most clinicians, it has been reported less nationally and internationally. At the earliest, Card first reported the disease in 1949, and in 1960, Zeive et al. in the U.S. again described hepatic myelopathy in detail, calling it post-shunt encephalomyelopathy. However, most of the cases reported in the relevant literature at home and abroad are disseminated cases, thus limiting the in-depth and systematic study of this disease. Pathogenesis of hepatic myelopathy At present, there is no uniform understanding of the pathogenesis of hepatic myelopathy. Most scholars believe that hepatic myelopathy is an irreversible pathological process, and there are two main doctrines regarding its pathogenesis: (1) Poisoning theory: due to the existence of artificial or spontaneous shunting between the portal veins, the toxic substances originating from the portal vein system will act on the brain and spinal cord without liver detoxification, resulting in the damage of neurons, axons and myelin sheaths. (2) Nutritional theory: Due to the existence of shunting between the portal veins, the metabolism of the liver itself is affected, resulting in a lack of nutrients necessary for the central nervous system. In turn, this leads to organic changes in the nervous system. Third, the clinical manifestations of hepatic myelopathy At present, domestic and foreign reports of hepatic myelopathy patients are mostly male, the age of onset is 23-68 years old, and hepatic encephalopathy often occurs before the onset of the disease. The main clinical manifestation is progressive spastic paralysis of both lower limbs, which is closely related to the formation of portal vena cava shunt or extensive spontaneous portal vena cava collateral circulation. The disease is generally categorized into 4 stages, as follows: (1) Pre-neurological symptoms: mainly chronic liver disease manifestations. (2) Subclinical hepatic encephalopathy stage: mainly characterized by poor computational ability and positive results of digital connectivity test and visual evoked potentials. (3) Hepatic encephalopathy stage: symptoms of hepatic encephalopathy may recur. (4) Spinal cord disease stage: Early manifestations of the patient are a feeling of heaviness in both lower limbs, difficulty in walking, scissor or spasmodic gait, which gradually develops into spastic paralysis of both lower limbs. Most of them only involve the lower limbs. A few develop spastic quadriplegia. Most of them have only motor disorders, and a few of them may have sensory disorders, visual changes or sphincter dysfunction. Limb symptoms are usually bilateral and symmetrical, manifested as elevated muscle tone, hypokinesia, and hyperreflexia. Fourth, the treatment of hepatic myelopathy (1) traditional treatment first treatment of all kinds of liver disease, should limit protein intake, oral lactulose to reduce intestinal ammonia absorption. Supplementation of menthol mono ornithine, monosodium glutamate, arginine and branched chain amino acids. Give high doses of vitamins B and C. Promote nerve regeneration. Coenzyme A, ATP, inosine, prostaglandins and compound danshen may promote nerve function recovery. Hyperbaric oxygen (HBO) treatment, so that the liver blood flow increases, brain tissue ammonia decreases, protection and repair of nerve myelin sheaths, has a certain efficacy on HM old. (2) Liver transplantationWith the increase in the number of cases of liver transplantation in patients with HM, there is more and more evidence that liver transplantation can significantly improve the symptoms. Liver transplantation can remove the root cause of the disease, which is favorable to the improvement of their symptoms. However, in patients who have developed spastic paralysis of the lower limbs, most scholars believe that it cannot improve their neurological damage. Some studies have reported that liver transplantation before the onset of hepatic spinal cord symptoms or no more than 10 months after the onset of symptoms has a better prognosis. The degree of improvement correlates with the time interval between the onset of spinal cord disease and liver transplantation. Therefore, the disease should be detected early, diagnosed early, and treated with liver transplantation in a timely manner. Early diagnosis and timely liver transplantation can stop the progression of the disease. However, when the disease forms irreversible damage, especially when it progresses to axonal degeneration, the disease becomes irreversible and the treatment effect is poor. Therefore, some scholars suggest that liver transplantation should be performed in time for patients with hepatic spinal cord, regardless of whether the liver function is in a state of decompensation or not. At present, there is no large case history statistics of liver transplantation for the treatment of this disease, and the clinical observation time is relatively short, so its exact efficacy needs to be further observed. However, from the recent clinical results, liver transplantation is a proven treatment method.