This case is described in Cushing's original Yale Registry[] and Cushing's article, “Peptic ulcers and the interbrain.”[] Patient 1, a 34-year-old man, presented in June 1915 with a 6-week history of unsteady gait associated with a 4-month history of nausea and vomiting. He also reported having midline suboccipital headaches starting in December 1914. The patient was diagnosed with a subcortical angioblastoma arising from the right cerebellar hemisphere. Cushing employed a bilateral suboccipital exploration that exposed both cerebellar hemispheres. He punctured the left lateral ventricle to lower the tension. Cushing reported “the dorsum and posterior clinoid processes show signs of pressure atrophy with destruction.”[] Pathologist W. T. Councilman diagnosed the intracranial mass as a “mixed tumor, possibly glioma-hemangioma.” Postoperatively, the patient described abdominal discomfort and vomited a bile-stained fluid. His postoperative abdominal exam showed it to be “somewhat spastic and with quite marked tenderness in the epigastrium.”[] Dr. Cushing admitted that not much attention was paid to the finding given the patient's “neurotic disposition” emerging from the effects of ether.\nDuring the evening, the patient had more severe cramp-like pain in the stomach with a rectal temperature of 102.4°. Morphine was administered multiple times. By early morning, the patient's temperature rose to 104°. Cushing described the patient as “cyanotic, breathing very rapidly and shallow and pulseless.” The patient died later that morning. Cushing's impression was an acute peritonitis of unknown origin.[]\nIt appears that pathologist W. T. Councilman had difficulty explaining the abdominal pathology and described “submucosa [as] hemorrhagic and appears to have been torn by mechanical violence… the muscularis is usually intact, but in many places, this also has ruptured… It is hard to explain the condition of the stomach, both gross and microscopically, except as a result of a mechanical action tending to stretch all layers.”[] According to the postmortem exam performed by Dr. J. L. Stoddard, the peritoneal cavity showed signs of fibrinous peritonitis in the upper abdomen and three circular gastric perforations between the cardia and pylorus. He reports that the gastric interior appeared to have been affected by corrosive poisoning.[]
Described in Cushing's original Yale Registry[] and Cushing's article, “Peptic ulcers and the interbrain,”[] Patient 2 was a 34-year-old man who presented with cerebellar signs and symptoms in November 1927. This was Dr. Cushing's second case of postoperative duodenal ulceration with perforation, 12 years after patient 1. Patient 2 reported a 5-year history of pain in the posterior neck and dizziness on bending over with diplopia, and said he had experienced weakness, numbness, and loss of control of his right arm and leg for about 10 months. He also reported four seizures, loss of consciousness, and a 3-year history of intermittent vomiting.\nOn exam, the patient had bilateral papilledema, ataxia, and sustained nystagmus. The patient was found to have a right partially cystic cerebellar astrocytoma. According to Dr. Cushing's operative note, the tumor could be easily separated from the cerebellar hemispheres via electrosurgery. A few days later, the patient experienced intense epigastric pain, and rectal temperature elevated to 102.4°. By the following morning, his temperature had risen to 106.2°. No vomiting had occurred, and he died 4 days postoperatively.\nAccording to Dr. G. A. Bennett, postmortem exam demonstrated a “residual mass of nonadherent tumor deeply indenting and flattening the medulla.” The peritoneal cavity had 1100 cc of a dark red-brown fluid and two irregularly-shaped perforations in the duodenal wall 3 cm from the pylorus. Microscopic examination of the tissue near the perforated areas demonstrated an acute inflammatory process and “showed a completely destroyed mucosa… replaced by an exudate of fibrin, inflammatory cells, and blood.”[] According to Bennett, these destructive lesions were the result of vascular thrombosis, commonly believed to be the cause of duodenal ulcers.[]