This case is described in Cushing's original Yale Registry[] and Cushing's article, “Peptic ulcers and the interbrain.”[] Patient 8, a 9-year-old girl, was admitted in September 1927 with an advanced cerebellar tumor syndrome. She had a 7-month history of frontal headaches, a 6-month history of projectile morning vomiting, weight loss, and ataxia. Physical exam also showed weakness of the upper branch of the left facial nerve, bilateral papilledema, and tortuous fundi vessels. Cushing suspected that a cerebellar tumor caused the increased intracranial pressure and papilledema.\nCushing proceeded with a bilateral suboccipital exposure and found the bone and dura covering the cerebellum to be thin. He inserted a needle into the left ventricle and fluid shot out of the manometer. Cushing found the tumor to have an interior cavity that contained “soft yellowish masses of degenerated tissue” and was able to separate the tumor from the fourth ventricle. Pathologist G.W. Bennett reported that the tumor “shows a pseudoadenomatous structure and a few pseudorosettes.”[] The child was found to have a median cerebellar medulloblastoma. For the next 2 years, the patient continued to vomit 2-3 times/week and experienced weight loss.\nThe patient was admitted again in July 1929 with complaints of headache, vomiting, and staggering gait, suggestive of increased intracranial pressure caused by a recurrence of the medulloblastoma. Exam showed positive Romberg, unsteady gait, nystagmus, and some forgetfulness. She improved with X-ray therapy and was discharged in August, but was readmitted in September. 10 days before admission, the patient had refused to feed herself, lost interest in her environment, and had urinary and fecal incontinence. She also was drowsy with daily vomiting and right occipital headaches. According to Dr. Oldberg, physical exam showed drowsiness, apathy, bilateral papilledema, right oculomotor palsy with diminution and/or disappearance of other deep reflexes. On October 10, 1929, an exploratory procedure was performed on the cerebellar region. The procedure was unable to show local recurrence. The first specimen showed “a mass of calcified, degenerated tissue.” Fluid from a lateral ventricular tap failed to show any tumor cells, but did show many red blood cells. On October 27, the patient fell into a coma with a temperature of 106.5° and died.\nAutopsy report notes “in the first portion of the duodenum approximately 3 cm below the pyloric sphincter, there is a small area which has a definite elevated margin with a depressed center forming more or less of a crater. The crater measures 3 cm × 4 cm in its greatest diameters… One section of the duodenum shows the ulcer… extends down to the muscularis, and its margins are deep… there is a narrow zone of dense hyalinized connective tissue… and some fibrin and red blood cells.”[]\nPostmortem examination of the patient's brain showed obstruction of the ventricular system by a recurrent medulloblastoma. Blood culture and brain base culture grew multiple colonies of Staphylococcus aureus which could indicate meningitis. Autopsy showed “very little purulent exudate over… cerebral hemispheres.”[]
Patient 10, a 10-year-old boy, presented with a 3-month history of ataxia and clumsiness, a 6-month history of dysarthria, and a 3-month history of suboccipital headaches and vomiting. Physical exam showed secondary optic atrophy, nystagmus, left facial nerve paresis, slurring of speech, and marked ataxia. Cushing suspected a cerebellar tumor. In surgery, there was a “protruding, bleeding, cavernous angioma which burst its way (through) the left cerebellar hemisphere as soon as an incision was made [through] the dura in spite of the ventricular puncture.”[] The patient's blood pressure fell rapidly. Postmortem examination of the mediastinum was performed on the operating room table following the patient's death. Cushing reported “the whole fatty contents of the mediastinum had been completely digested away leaving the aorta exposed, the plexus of sympathetic nerves free and naked as though they had been dissected out.”[] Cushing also wrote that a 1-inch slit was found in the esophagus, allowing gastric contents to “leak out.” He reported: “I cannot believe that the perforation in this child was due to anything else than a digestive ulcer of the esophagus… the dissection appearance of the structures in the mediastinum was much more likely to have been produced by a digestive process…”[] This patient was also mentioned in Cushing's paper, “Peptic ulcers and the interbrain,” in which he discussed 11 patients suffering from both intracranial and gastric lesions.[]