Cushing ulcer is an acute gastro-duodenal ulcer that can develop within hours of a traumatic brain injury. The pathology is debated. Explanations include acid damage resulting from increased parietal cell activity mediated by the vagus nerve, and a decrease in protective mucus production. These days, the condition is efficiently prevented in critically ill patients by decreasing acid production with antacids and histamine-2 receptor blockers.
Cushing ulcer, which can form in the stomach, duodenum, or esophagus, is a complication of traumatic brain injuries. It develops very quickly (possibly within hours) following trauma. It is often discussed in the context of stress ulcers  and manifestations of stress gastritis (originally called neurogenic gastritis), but it has some characteristics not shared by other stress ulcers. Stress ulcers in general manifest as a number of superficial lesions in the gastric mucosa, whereas Cushing ulcer is usually solitary and deep, and therefore carries a high risk of perforation. Another distinguishing feature of Cushing ulcers is that it is associated with increased levels of gastrin and pepsin . The pathophysiology of the condition is not completely clear but is likely to be due to the effects of elevated intracranial pressure following brain injury  with consequent increased gastric acid production due to stimulation of the vagus nerve .
The three patients described in the original 1932 paper of Cushing   had cerebellar tumors and died after surgery due to perforative peritonitis. They had symptoms of bloating and abdominal sensitivity, or severe abdominal pain, or brown vomit. The occurrence of ulcers in patients with an intracranial disease was observed almost a century earlier by Rokitansky, hence the disease is often referred to as Rokitansky-Cushing ulcer. Presentation with sudden fever, leukocytosis, and volume contraction in the presence of increased intracranial pressure and high-dose corticosteroid administration were suggested as diagnostic clues for perforated stress ulcer by Walsh et al.  for aphasic patients. The lesions have about a 17% risk of bleeding  .
Acute stress gastritis following brain injury has been on the decline since the introduction of prophylaxis using antacids and histamine-2 receptor antagonists  . Nevertheless, the condition still occurs for various reasons, one of which is a large number of head injuries due to traffic accidents . Cushing ulcer sometimes develops in spite of ulcer prophylaxis, as in the case of an 8-month old infant with medulloblastoma who became afflicted with the condition once a preoperative dexamethasone treatment was initiated .
Perforation of a Cushing ulcer should be anticipated in patients with brain injuries .
Upper gastrointestinal endoscopy is the most sensitive technique for the detection of gastric and duodenal ulcers. Endoscopy can also be used to obtain biopsy samples for cytological examination, or for testing for Helicobacter pylori infection. Radiography is useful for the detection of free air in the abdomen, an indication of perforation; however, the absence of free air does not exclude the possibility of perforation . Angiography is used in patients who have massive bleeds. Various laboratory parameters are performed, for example, serum gastrin levels.