Association of venous angioma and atypical meningioma--case report.
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A 67-year-old male presented with an atypical meningioma arising from the right tentorium associated with a venous angioma in the left cerebellar hemisphere. The venous angioma was detected incidentally during examinations for the brain tumor. The brain tumor was removed completely and the venous angioma followed conservatively. Venous angiomas associated with brain tumors should be followed conservatively, as the clinical significance and surgical indications are unclear. (+info)
Paediatric presentation of type 2 neurofibromatosis.
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BACKGROUND: Neurofibromatosis type 2 (NF2) is a highly penetrant autosomal dominant condition predisposing affected individuals to schwannomas and meningiomas. The proportion of children presenting with meningioma or schwannoma who have NF2 is not well described, and neither is the mode of presentation in most children with the inherited disease. AIMS: To determine the frequency of childhood meningioma and schwannoma cases caused by NF2 and the mode of presentation. METHODS: The records of the Manchester Children's Tumour Registry from 1954 were searched for cases of meningioma and schwannoma. Paediatric presentation in a large UK series of NF2 was also studied. RESULTS: 18% (61/334) of patients with NF2 on the UK database presented in the paediatric age group (0-15 years), frequently with the symptoms of an isolated tumour. More than half had no family history to alert the clinician to their susceptibility. Three of 22 children presenting with a meningioma on the Manchester Children's Tumour Registry have gone on to develop classic features of NF2. CONCLUSIONS: Clinicians should suspect NF2 in children presenting with meningioma, schwannoma, and skin features, such as neurofibromas/schwannomas, but fewer than 6 cafe au lait patches, who thus fall short of a diagnosis of neurofibromatosis type 1. (+info)
Combined fat- and water-suppressed MR imaging of orbital tumors.
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BACKGROUND AND PURPOSE: The use of a high-resolution T2-weighted MR sequence, which suppresses signal from both fat and water, has been shown to be highly effective for depicting areas of inflammatory damage within the optic nerve. The ability of this sequence to show neoplastic and inflammatory orbital lesions, which may mimic neuritis, is unknown. This study was designed to examine the characteristics of such a sequence for the investigation of orbital mass lesions. METHODS: Twenty-eight patients with known or suspected mass lesions of the orbit and six healthy volunteers were recruited for study. Imaging was performed with a 1.5-T MR unit. Participants were examined by selective partial inversion recovery (SPIR) sequences with T2-weighted fast spin-echo acquisition, selective partial inversion recovery/fluid attenuated inversion recovery (SPIR/FLAIR) sequences with fast spin-echo acquisition, short tau inversion recovery (STIR) sequences with fast spin-echo acquisition, and SPIR sequences with contrast-enhanced T1-weighted fast spin-echo acquisition. Two neuroradiologists, using a randomised, blinded method, scored images for lesion presence and extent. Lesion extent was defined as the number of images with visible abnormality, and was compared with the standard of reference established at a later date by consensus review of all imaging sequences. The ability of the sequences to show the presence and extent of pathologic lesions was compared. RESULTS: The SPIR/FLAIR sequence showed both the presence and extent of orbital masses significantly better than did either STIR or T2-weighted SPIR sequences (P<.01 and P<.001, respectively). Contrast-enhanced T1-weighted SPIR images ranked better than SPIR/FLAIR images, although the difference failed to reach statistical significance. In the orbital apex, the SPIR/FLAIR technique was superior to all other techniques used. This reflected its ability to distinguish enhancing, pathologic lesions from enhancing, normal anatomy. CONCLUSION: SPIR/FLAIR is an appropriate screening technique for orbital masses and offers significant advantages over currently used fat-suppressed sequences for the investigation of orbital disease. (+info)
Five novel immunogenic antigens in meningioma: cloning, expression analysis, and chromosomal mapping.
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Tumorigenesis of meningioma has been associated with chromosome 22, most notably the NF2 gene, but additional genes have been implicated in meningioma development. Here, we report the identification of five novel immunogenic antigens expressed in meningioma. An expression library was generated from a meningioma that retained both copies of chromosome 22. Screening with autologous patient serum identified seven cDNA clones that were indicated by antigen-antibody complexes. The clones were sequenced, and sequence comparison revealed that the seven clones represent five different genes, providing evidence that meningiomas express a spectrum of immunoreactive antigens, which were termed meningioma expressed antigens (MGEAs). One gene was identical with the connective tissue growth factor, one gene was in part homologous to an Alzheimer disease-associated gene, and a third gene was in part identical to Homo sapiens molybdenum cofactor biosynthesis proteins A and C mRNA. One gene was partially homologous to previously reported cDNA sequences of unknown function, and the fifth gene showed no significant homologies to sequences deposited in databases. Using somatic hybrid mapping, three genes were localized on chromosome 6, and two genes were localized on chromosomes 3 and 17, respectively. To distinguish the MGEAs from the so-called natural autoantigenes, we also screened the library with 12 sera from individuals without obvious disease. The clones identified by reactivity with normal sera were completely different from the clones identified by screening the same meningioma expression library with serum from the patient bearing the tumor. These data suggest that the newly identified MGEA genes may be useful for diagnosis and possibly therapy of meningioma. (+info)
Deletion of chromosome 1p and loss of expression of alkaline phosphatase indicate progression of meningiomas.
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Meningiomas are cytogenetically characterized by loss of one chromosome 22 as a typical primary aberration and progression-associated secondary chromosome changes, of which monosomy 1p is the most common. The aim of this study was to evaluate the significance of monosomy 1p and enzyme activity loss of tissue nonspecific alkaline phosphatase (ALPL), whose gene maps to chromosome 1p36.1-p34, as parameters for the diagnosis of progression-prone meningiomas. We analyzed smear preparations of 56 meningiomas and additional paraffin sections of 17 of the cases by two-color fluorescence in situ hybridization (FISH) using the D1Z1 and D1Z2 probes and by a metaphase cytogenetic analysis of 30 of these tumors. The results were compared to clinical and morphological parameters and the expression of ALPL. Smear preparations showed deletion of 1p36 in 27% of common-type, 70% of atypical (intermediate-type), and 100% of anaplastic meningiomas. Monosomy 1p, as detected by FISH or the karyotype, was strongly associated with complete loss of ALPL activity. Intermediate-type and anaplastic meningiomas of younger patients displayed an increasing rate of cells with trisomy 1q and relative loss of 1p. The highly significant correlation of FISH results and ALPL histochemistry with clinical parameters gives evidence of their strong prognostic relevance. The complete activity loss of ALPL and the immunologically detected loss of ALPL protein in areas of meningiomas with monosomy 1p indicate a cytogenetically undetectable inactivation of the homologous Alpl allele. The apparently homozygous loss of expression of ALPL supports the notion that Alpl is a candidate tumor suppressor gene in meningiomas. (+info)
Natural history of elderly patients with asymptomatic meningiomas.
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OBJECTIVE: For the treatment of elderly patients with asymptomatic meningiomas, it is important to determine their natural history. Based on results of follow up examinations, the natural history of such patients was clarified and prognostic factors concerning the potential of tumour growth in the aged were identified. METHODS: The clinical records and imaging studies of 40 elderly (over 70 years) patients with asymptomatic meningiomas were analysed. The patients were followed up with repeated imaging studies, and changes in tumour size, clinical signs, and outcomes were evaluated. RESULTS: There were 32 women and eight men with a mean age of 76.1 years. The mean follow up period was 38.4 months, ranging from 6 to 97 months. Six patients died during the follow up period from disorders other than the tumours, and one patient died as a result of the tumour. Twenty six patients (mean follow up period 41.8 months, range 10-97 months) showed no tumour growth. Fourteen patients showed tumour growth (mean follow up period 32.1 months, range 6-88 months). Five (four men and one woman) of these patients became symptomatic. Based on imaging analysis (1) calcification of the tumour was associated with no tumour growth (p=0.036), and (2) the tumour size at the initial diagnosis was related to subsequent tumour growth (p=0.016). Other possible factors related to tumour growth included sex and hyperintensity on MRI T2 weighted images. CONCLUSION: In elderly patients with asymptomatic meningiomas, careful clinical follow up with imaging studies is important. The imaging features mentioned may contribute to prediction of tumour growth. (+info)
Tight association of loss of merlin expression with loss of heterozygosity at chromosome 22q in sporadic meningiomas.
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Mutations of NF2, the gene for neurofibromatosis 2, are detected in 20-30% of sporadic meningiomas, and almost all mutations lead to loss of merlin expression. However, loss of heterozygosity (LOH) at chromosome 22q is found at a much higher frequency, up to 50-70%, and the possibility of another tumor suppressor gene in this region has not been excluded. Furthermore, a recent report proposed that abnormal activation of a protease micro-calpain can be an alternative pathway for merlin loss in meningiomas and schwannomas. To determine the correlation of merlin loss with NF2 genetic alteration or micro-calpain activation, we performed a molecular genetic analysis of 50 sporadic meningiomas and also examined the expression status of merlin and active form micro-calpain. LOH assay of five microsatellite markers franking NF2 revealed LOH in 22 cases, and single-strand conformation polymorphism assay detected six frameshift mutations, two splicing mutations, one nonsense mutation, and one missense mutation, all accompanied by 22q LOH. In addition, a multiplex PCR assay indicated homozygous deletion of NF2 in two cases. Interestingly, a marked decrease of merlin expression was seen exclusively in the 22 cases with 22q LOH. Activated micro-calpain expression was observed in 28 cases at various levels but showed no correlation with merlin status. These data strongly support the notion that NF2 is the sole target of 22q LOH in meningiomas and that loss of merlin expression is always caused by genetic alteration of NF2, following the classic "two hit" theory. (+info)
Midline and far lateral approaches to foramen magnum lesions.
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Twenty patients with foramen magnum lesions were operated upon in the last 5 years at Postgraduate Institute of Medical Education and Research, Chandigarh. The common presenting features were quadriparesis, quadriplegia, diminished sensations, neck pain and respiratory insufficiency. The lesions encountered were meningiomas, neurofibromas, posterior inferior cerebellar artery aneurysms, neurenteric cyst and chordoma. Patients with posterior or posterolaterally placed lesions were operated by the midline posterior approach while those with anterior or anterolateral lesions were managed by the far lateral approach. All mass lesions were excised completely and the aneurysms were clipped. Seventeen patients made good neurological recovery while three died. The latter three patients presented very late. The merits of various surgical approaches to the foramen magnum are discussed. (+info)