There has been continuing debate on the subject of malignant meningiomas, but few studies of large series have been reported. We present our experiences with 25 atypical and malignant meningiomas operated on at Henry Ford Hospital between 1976 and 1990. A total of 319 primary intracranial meningiomas were operated on during this period; of these, 294 (92%) were benign, 20 (6.26%) atypical, and 5 (1.7%) malignant. We used a modified histological grading system, based primarily on World Health Organization criteria of malignancy (hypercellularity, loss of architecture, nuclear pleomorphism, mitotic index, tumor necrosis, and brain invasion), to define atypical and malignant meningiomas. Each of these criteria was given a score from 0 to 3, and then partial scores were added to obtain cumulative scores. These total scores were then used to determine what is benign, atypical, and malignant. The peak incidence of atypical and malignant meningiomas was in the seventh and sixth decades, respectively. The predominance of female patients with benign meningiomas was not observed in the nonbenign group. The male:female ratio for atypical and malignant meningiomas was 1:0.9 versus 1:2.3 for benign meningiomas (P = 0.024). The most common presenting symptom and physical sign in our patients was paresis. In reviewing their radiographic features, all patients showed moderate or marked edema on computed tomography. Calcification was exhibited by one patient only and "mushrooming" was seen in three cases. Of the 25 patients, 11 (44%) died during follow-up: 2 in the perioperative period, 8 within the first 5 years, and 1 died 11 years after the diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Primary sclerosing cholangitis (PSC) is a progressive, cholestatic disease of the liver that is marked by inflammation of the bile ducts and damage to the hepatic biliary tree. Approximately 60–70% of patients also have inflammatory bowel disease and progression of PSC can lead to ulcerative colitis and cirrhosis of the liver. Due to limited understanding of the etiology and mechanism of PSC, the only existing treatment option is orthotopic liver transplantation (OLT); however, recurrence of PSC, after OLT is estimated to be between 5% and 35%. We discuss the successful treatment of a pediatric patient, with recurrent PSC, after OLT with oral Vancomycin.

Four examples of human cerebral medulloepithelioma were studied immunohistochemically with a panel of antibodies and antisera to neuronal and glial proteins. The tumors, in addition to primitive medullary epithelium, contained areas of neuroblastic, ganglionic, astrocytic, ependymoblastic and ependymal differentiation, and in one tumor, areas resembling polar spongioblastoma. Tumor cells throughout the primitive medullary epithelium displayed focal immunoreactivity for vimentin, glial fibrillary acidic (GFA) protein and for the neuron-associated class III beta-tubulin isotype. Neuroblasts showed immunoreactivity for the class III beta-tubulin isotype, microtubule-associated protein 2 and neuron-specific enolase. Immunoreactivity for neurofilament epitopes and synaptophysin was detected in areas of ganglionic differentiation and coincided with the demonstration of neurofibrils in Bielschowsky's silver impregnations. Vimentin was the only marker detected in ependymoblastic and ependymal rosettes or in areas of polar spongioblastoma, as well as in mesenchymal cells. The results indicate that, even in very primitive neoplastic neuroepithelium, immunocytochemical evidence of early commitment of some of the cells to a neuronal or glial lineage can be demonstrated. The neuron-associated class III beta-tubulin isotype appears to be one of the earliest markers indicative of neuronal differentiation in normal and neoplastic primitive neuroepithelium.

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There has been continuing debate on the subject of malignant meningiomas, but few studies of large series have been reported. We present our experiences with 25 atypical and malignant meningiomas operated on at Henry Ford Hospital between 1976 and 1990. A total of 319 primary intracranial meningiomas were operated on during this period; of these, 294 (92%) were benign, 20 (6.26%) atypical, and 5 (1.7%) malignant. We used a modified histological grading system, based primarily on World Health Organization criteria of malignancy (hypercellularity, loss of architecture, nuclear pleomorphism, mitotic index, tumor necrosis, and brain invasion), to define atypical and malignant meningiomas. Each of these criteria was given a score from 0 to 3, and then partial scores were added to obtain cumulative scores. These total scores were then used to determine what is benign, atypical, and malignant. The peak incidence of atypical and malignant meningiomas was in the seventh and sixth decades, respectively. The predominance of female patients with benign meningiomas was not observed in the nonbenign group. The male:female ratio for atypical and malignant meningiomas was 1:0.9 versus 1:2.3 for benign meningiomas (P = 0.024). The most common presenting symptom and physical sign in our patients was paresis. In reviewing their radiographic features, all patients showed moderate or marked edema on computed tomography. Calcification was exhibited by one patient only and "mushrooming" was seen in three cases. Of the 25 patients, 11 (44%) died during follow-up: 2 in the perioperative period, 8 within the first 5 years, and 1 died 11 years after the diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracytoplasmic lumina (ICL) are rarely described in tumors of the central nervous system. The morphogenesis of ICL remains incompletely characterized. Ultrastructural features of ICL in six ependymomas (one from lateral ventricle, three from fourth ventricle, and two from spinal cord) and three myxopapillary ependymomas of the filum terminale were analyzed. Two types of ICL were identified: ICL with both microvilli and cilia, and ICL with only microvilli. Some ICL also contained granulofibrillary or condensed material. Ciliated ICL were common in ependymomas of the ventricles, whereas nonciliated ICL were frequently seen in the myxopapillary variant. Various stages of formation and development were observed in ciliated ICL. They seemed to originate from distended periciliary cisterns, to enlarge by fusion with cytoplasmic vesicles or other ICL, and subsequently to open into the intercellular space. The last process may be the mechanism by which the intercellular microrosettes are formed. Ciliated ICL have not been described in other neoplasms. They may represent a characteristic ultrastructural feature of ependymomas. The morphogenesis of nonciliated ICL remains unknown. They may represent a degenerative form of ciliated ICL or pseudolumina resulting from invagination of the extracellular space within the cytoplasm.

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