Symptomatic suprasellar endodermal cyst, possibly originating from the Seessel's pouch, containing fluid with a high carcinoembryonic antigen level.

A 32-year-old man presented with a rapidly progressive decrease in visual acuity and diplopia. Magnetic resonance imaging (MRI) revealed a suprasellar cystic mass extending to the upper part of the clivus. The content of this cyst showed a slightly higher signal intensity than that of his cerebrospinal fluid (CSF) on T1-weighted images. The cyst stretched the pituitary stalk, but a normal pituitary signal was observed. The cyst wall was maximally resected under neuroendoscopy, which yielded fluid contents that were white and mucous like, with a carcinoembryonic antigen (CEA) level 1,400 ng/ml or higher. On light microscopy, one to two layers of epithelial cells with cylindrical nuclei on loose connective tissue lined the cyst cavity. These cells were positive for periodic acid-Schiff, CEA, and cytokeratin 7 and negative for cytokeratin 20. On electron microscopy, epithelial cells showed many short microvilli with coating material. The cytoplasm was rich in electron-dense material, and dense intercellular adhesion was observed, but neither goblet cells nor cilia were present. On the basis of MRI features, cytokeratin expression patterns and electron microscopic findings, the patient was considered to have a suprasellar endodermal cyst derived from Seessel's pouch.

Colloid cysts of the third ventricle. Endoscopic and open microsurgical management.

BACKGROUND AND PURPOSE: The endoscopic approach to colloid cysts of the third ventricle is receiving increasing interest. However, its effectiveness is a matter of discussion. The aim of the study was to present direct and long-term outcome after endoscopy of colloid cyst vs microsurgery. MATERIAL AND METHODS: Medical records of 23 patients with colloid cysts were retrospectively analyzed. This group consists of 10 patients treated endoscopically and 13 patients treated using a transcortical-transventricular approach. Sex and age distributions were similar in both groups. Clinically, symptoms of raised intracranial pressure predominated. All patients had hydrocephalus. Tumour diameter ranged from 1.5 to 3 cm. Mean follow-up period was 31 months. RESULTS: In 6/10 endoscopically treated patients, tumours were completely removed. In 3 patients, small capsule remnants, adherent to the choroid plexus and veins, were left. In one case, a portion of capsule, obstructing the intraventricular foramen, was finally removed microsurgically. Postoperatively, 2 patients complained of memory deficits, which became permanent in one case. One patient developed temporary mutism. In one case, with symptoms of hydrocephalus without colloid cyst recurrence, a ventriculoperitoneal shunt was implanted 6 months after the initial surgery. In all microsurgically treated patients tumours were completely removed. One patient was reoperated because of intracerebral haematoma. Two patients suffered from temporary hemiparesis and 2 developed epilepsy. Within one year after surgery 3 patients were shunted because of hydrocephalus; one patient required antiepileptic treatment. CONCLUSIONS: The endoscopic approach to colloid cysts of the third ventricle is safe, effective and carries a low complication rate. Endoscopy may be recommended as a treatment option.

Vascular endothelial growth factor (VEGF) is elevated in brain tumor cysts and correlates with tumor progression.

Vascular endothelial growth factor (VEGF), a key regulatory protein in neoangiogenesis, is strongly expressed in a variety of primary brain tumors, particularly malignant gliomas. In previous studies, high levels of VEGF were also reported in tumor cysts of glioblastomas. Using an ELISA method we measured the concentration of VEGF in matched samples of aspiration fluid from tumor cysts and serum. Samples were collected from 14 patients with primary brain tumors of various histology (six glioblastomas, one protoplasmatic astrocytoma, two pilocytic astrocytomas, one ependymoma, one meningioma, and three craniopharyngiomas) and two patients with solitary cystic brain metastases from adenocarcinomas of the lung. Aspiration fluids of tumor cysts from all patients revealed high VEGF levels ranging between 882 and 1,263,000 pg/ml, which were 2 to more than 2,000 times higher than the corresponding serum levels. Maximum VEGF levels were detectable in cyst fluids from recurrent glioblastoma. Serum VEGF levels ranged between 125 and 716 pg/ml and did not differ from serum levels in 145 healthy volunteers. In a single patient with metastatic lung cancer the concentration of VEGF in serum and cyst fluid was determined during disease progression. During 60 days of follow-up VEGF concentrations in the cyst fluid collected by puncture of an Ommaya reservoir increased 650-fold, while serum levels remained rather constant. These findings indicate that immunoreactive VEGF is produced at the tumor site and abundantly released into the cyst fluid of primary and metastatic brain tumors. Interestingly, this abundant local release is not reflected in serum VEGF levels, even in the case of very high VEGF concentrations in tumor cysts. Thus, VEGF may be biologically relevant for the formation of tumor cysts in brain tumors and correlates with local disease progression.