Wernicke’s (WE) encephalopathy is an encephalopathy caused by vitamin B1 (thiamine) deficiency first discovered by Carl Wernicke in 1881. It is mostly seen as a metabolic encephalopathy caused by thiamine deficiency due to chronic ethanolism caused by long-term heavy alcohol consumption. Causes of thiamine deficiency include vomiting in pregnant women, malnutrition, anorexia nervosa, liver disease, total gastrectomy, jejunostomy, gastric cancer, malignancy, pernicious anemia, chronic diarrhea, long-term renal dialysis, non-intestinal nutritional deficiency of thiamine, long-term rehydration, and magnesium deficiency. Animal experiments have shown that chronic alcohol intoxication can lead to malnutrition, mainly thiamine deficiency, which in turn can aggravate chronic alcohol intoxication. The proportion of patients with non-ethanol intoxication is reported to be 39% to 50%, those with acute pregnancy vomiting, those with acute pancreatitis temporary fasting, and those with total parenteral nutrition after surgery are also more common. Early supplementation of vitamin B1 is the key to the treatment of this disease. Patients who are diagnosed and treated in time can recover completely, and the death rate is 10% to 20%. The age of onset is 30-70 years old, with an average of 42.9 years old and slightly more males. Only 1/3 of patients have typical clinical manifestations of the triad (i.e. extraocular muscle paralysis, ataxia, mental and consciousness disorders), and most patients have advanced complications of various related diseases, with a high rate of clinical misdiagnosis. Wernicke’s encephalopathy has an atypical clinical presentation, and MRI is an ideal tool for diagnosing Wernicke’s encephalopathy and can help in the early diagnosis of Wernicke’s encephalopathy. The signal is slightly low in T1WI, high in T2WI and high in DWI. The typical change in the acute phase is symmetric T2WI high signal around the third ventricle and aqueduct, and after 6-12 months, the high signal decreases or disappears in the recovery phase; papillary body atrophy is the characteristic neuropathological abnormality of Wernicke’s encephalopathy, and the marked reduction of papillary body volume is not only a specific sign of thiamine deficiency, but also a distinguishing feature between Wernicke’s encephalopathy and Alzheimer’s disease. The disease is easily overlooked because of its extremely neurological-like pathogenesis. For the diagnosis of this disease, it is crucial to think about it. It is cautioned that for patients with long-term alcoholism or long-term fasting, once the three main symptoms of nystagmus, somatic ataxia and mental disorders appear, they must not forget to take vitamin B1 supplements in time and be alert to the occurrence of Wernicke’s encephalopathy.