Abstract

Computed tomography (CT) of the head revealed localized osteosclerotic thickening in the left temporo-parietal bone, with spiculated margins of the inner and outer tables, involving the coronal suture and extending to the frontal bone, with no evident bony erosion. Magnetic resonance imaging (MRI) showed an expansile hypointense lesion on the T1and T2-weighted images in the left temporo-parietal bone with thickening of the extracranial soft tissues and no associated intracranial lesions. Wide surgical resection of the lesion was carried out with cranioplasty. Histopathological examination showed clusters of meningothelial cells, forming small whorls and infiltrating the trabecular bone spaces, which gave the diagnosis of intraosseous calvarial meningioma (ICMs). Intraosseous calvarial meningiomas are defined as meningiomas confined to the skull with no dural involvement [1, 2]. Meningiomas arising outside the dural compartment have been called ectopic, extracranial, extradural, calvarial, extraneuraxial, or intraosseous meningiomas. To avoid the confusion in nomenclature, Lang et al. has proposed a single term, primary extradural meningiomas (EDMs), for such lesions [3]. Primary EDMs have an incidence of less than 2 % of all meningiomas [3–7] and have been reported to arise from the scalp tissue, orbit, paranasal sinuses, nasopharynx, salivary glands, neck, skin, lung, mediastinum, adrenal and paraspinal regions, and even the fingers [3–5]. Primary EDMs have a slight female preponderance (1:1.4) with a bimodal age distribution, the first peak being in the 2nd decade and the next in the 5th to 7th decades [1, 3–5]. Intraosseous meningiomas are exceedingly rare, forming 14 % of all cases of primary EDMs [6, 7]. The calvarium is involved in 68 % of intraosseous meningiomas, with the fronto-parietal and orbital regions being the commonest locations [1, 3, 5, 6]. Several explanations are proposed in the literature for the probable origin of ICMs. They are thought to arise from ectopic meningocytes or arachnoid cap cells trapped in the cranial sutures during molding of the head at birth. A second explanation is post-traumatic misplacement or entrapment of meningothelial cells into suture or fracture lines. A third explanation is that meningiomas may develop from multipotential mesenchymal cell precursors, thus explaining the occurrence of meningiomas in uncommon locations [1, 5, 6]. An association of ICM with neurofibromatosis type II has been reported in a case by Poptodorov et al., in which ICM and spinal meningioma were the initial manifestations of this disease [8]. The commonest presenting feature of ICM is a gradually expanding painless mass [1, 3–5, 7], usually benign and slow-growing. However, it is reported that ICMs are more prone to developing malignant changes The case presentation can be found at doi: 10.1007/s00256-014-1984-5

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