The primary causes of hepatic encephalopathy include severe viral hepatitis, severe toxic hepatitis, drug-induced liver disease, acute fatty liver in pregnancy, various types of cirrhosis, post portal-body vein shunt, primary liver cancer, and other end-stages of diffuse liver disease, and hepatic encephalopathy occurs most frequently in patients with cirrhosis, which accounts for about 70% of cases. There are many factors that induce hepatic encephalopathy, such as upper gastrointestinal bleeding, high protein diet, large amount of potassium drainage diuretic, ascites release, use of sleeping, sedative, anesthesia, constipation, uremia, infection or surgical trauma and so on. Then, how to check for proximal coma? The following is an introduction to proximal coma examination methods: 1, laboratory tests: (1) abnormal liver function, abnormal coagulation function. (2) Blood ammonia measurement. (3) plasma amino acid measurement. 2.Electroencephalogram examination: the changes of electroencephalogram have certain significance to the diagnosis and prognosis of this disease. Normal EEG wave amplitude is low, frequency is fast, and wave pattern is alpha; wave. With the change and development of the disease, the frequency slows down, the wave amplitude gradually increases, and the wave pattern changes from alpha;wave to theta;wave of 4-7 times per second, which is suggestive of pre-comatose stage, such as changing into symmetrical, high amplitude, delta;wave of 1.5-3 times per second, which is the manifestation of comatose stage. Suspected EEG changes can be clarified by increasing EEG changes after high protein intake and small doses of intramuscular morphine. Electroencephalographic changes in hepatic encephalopathy can also be seen in uremia, pulmonary failure and hypoglycemia, etc., and should be distinguished. 3.Visual-evokedpotential（VEP）：Stimulation with flash of light can make the cortex of visual area of occipital lobe stimulate the response and produce synchronous discharge effect, which will cause potential changes, i.e. VEPs, which represents the sum of post-synaptic excitation and inhibition potentials of the cortical and subcortical nerve cell populations. It is specific for assessing brain dysfunction in hepatic encephalopathy and can be quantitatively analyzed. It reflects brain potential activity more accurately than general EEG and can be used to detect hepatic encephalopathy before the onset of symptoms (e.g., subclinical hepatic encephalopathy). In addition, some people apply auditory event-related potential P300 and somatosensory evoked potentials to diagnose subclinical hepatic encephalopathy, and believe that the diagnostic value of auditory event-related potential P300 is more sensitive and specific than somatosensory evoked potentials. 4. Brain-conducted magnetic stimulation test: Nolano et al. applied brain-conducted magnetic stimulation to determine the cortical motor function of cirrhotic patients, and found that the central motor nerve conduction time was prolonged, the motor arousal threshold was increased during sleep, the central non-recording period was shortened, and the periphery was normal, which indicated that there was already damage to the corticospinal pathway, and this could be regarded as the preexisting manifestation of cirrhosis and hepatic encephalopathy.