A consecutive series of 23 patients underwent operative removal of an intramedullary spinal cord ependymoma between January, 1976, and September, 1988. Thirteen women and 10 men between the age of 19 and 70 years experienced symptoms for a mean of 34 months preceding initial diagnosis. Eight patients had undergone treatment prior to tumor recurrence and referral. Mild neurological deficits were present in 22 patients on initial examination. The location of the tumors was predominantly cervical or cervicothoracic. Radiological evaluation revealed a wide spinal cord in all cases. Magnetic resonance (MR) imaging was the single most important radiological procedure. At operation, a complete removal was achieved in all patients. No patient received postoperative radiation therapy. Histological examination revealed a benign ependymoma in all cases. The follow-up period ranged from 6 to 159 months (mean 62 months) with seven patients followed for a minimum of 10 years after surgery. Fourteen patients underwent postoperative MR imaging at intervals ranging from 8 months to 10 years postoperatively. No patient has been lost to follow-up review and there were no deaths. No patient showed definite clinical or radiological evidence of tumor recurrence during the follow-up period. Recent neurological evaluation revealed functional improvement from initial preoperative clinical status in eight patients, no significant change in 12 patients, and deterioration in three patients. The data support the belief that long-term disease-free control of intramedullary spinal ependymomas with acceptable morbidity may be achieved utilizing microsurgical removal alone.

Together, these results demonstrate that human gliomas contain multiple populations of cells with the capacity to form tumors and specifically identify a population of tumorigenic A2B5+ cells that are phenotypically distinct from CD133+ cells.

Subtle cognitive decline following CEA occurs and persists for at least several weeks after surgery. This decline was absent in a control group.

Four patients with metastatic carcinoma to the pituitary gland are presented. Two of these patients had no previous history of malignancy and, based on clinical, laboratory, and radiological evaluation, a preoperative diagnosis of pituitary adenoma was made. In one patient, the histological diagnosis of two consecutive tumour specimens, obtained 1 year apart, was pituitary adenoma. The correct diagnosis of metastatic renal-cell carcinoma was not ascertained until autopsy. In the second patient, a diffusely infiltrating breast carcinoma was diagnosed by mammography and confirmed by biopsy, after pathological examination of the sellar tumour revealed carcinoma. The third patient underwent mastectomy 3 years earlier for breast carcinoma and had known metastatic disease. The fourth patient had known metastatic endometrial carcinoma when she became symptomatic from a pituitary metastasis. The incidence, clinical features, and pathophysiology of metastatic carcinoma to the pituitary gland are discussed.