AIM: To explore the etlology, pathogenesis, diagnosis, and treatment of postsurgical gastroparesis syndrome (PGS) after pancreatic cancer cryotherapy (PCC) or pancreatico-duodenccomy (PD), and to analyze the correlation between the multiple factors and PGS caused by the operations. METHODS: Clinical data of 210 patients undergoing PD and 46 undergoing PCC were analyzed retrospectively. RESULTS: There were 31 (67%, 31/46) patients suffering PGS in PCC group, including 29 with pancreatic head and uncinate tumors and 2 with pancreatic body and tall tumors. Ten patients (4.8%, 10/210) developed PGS In PD group, which had a significantly lower Incldence of PGS than PCC group (χ=145, P<0.001). In PCC group, 9 patients with PGS were managed with non-operative treatment (drugs, dlet, nasogastric sucion, etc.), and one received reoperation at the 16th day, but the symptoms were not relieved. In PD group, all the patients with PGS were managed with non-operative treatment. The PGS in patients undergoing PCC had close assoclation with PCC, tumor location, but not with age, gender, obstructive jaundice, dypoproteinemia, preoperative gastric outlet obstruction and the type and number of gastric biliary tract operations. The mechanisms of PGS caused by PD were similar to those of PGS following gastrectomy. The damage to interstitial cells of Cajal might play a role in the pathogenesis of PGS after PCC, for which multiple factors were posslbly responsible, including ischemic and neural injury to the antropyloric muscle and the duodenum after freezing of the panctaatico-duodenal regions or reduced circulating levels of motilin. CONCLUSION: PGS after PCC or PD is induced by multiple factors and the exact mechanisms, which might differ between these two operations, remain unknown. Radiography of the upper gastrointestinal tract and gastroscopy are main diagnostic for PGS, and reoperation should be avolded in patients whith PGS caused by PCC.