Supratentorial calcified pseudotumour: experience of a single institution and review of the literature

Abstract

Surgical removal is recommended for benign intracranial CPTs that are symptomatic, are associated with brain oedema, or show tumour growth. Stable and asymptomatic CPTs can be followed.

Calcifying pseudoneoplasm of the neuraxis in direct continuity with a low‐grade glioma: A case report and review of the literature

“…In previous reports, CT images of CAPNON typically showed solid calcifications, and MRI often revealed a well‐defined lesion that was uniformly hypointense on both T1‐ and T2‐weighted images without perilesional edema . Only five cases have shown surrounding T2 hyperintensity suggestive of local edema or tumoral invasion . Gadolinium‐enhanced MRI also showed minimal rim enhancement of the tumor .…”

“…The most characteristic radiological feature of CAPNON is dense calcification . For intracranial lesions, differential diagnoses include astrocytoma, oligodendroglioma, choroid plexus papilloma, meningioma, craniopharyngioma, ependymoma, cavernous angioma, chondrosarcoma, chondroblastoma, chondroma, calcified metastatic brain tumor and tuberculoma . In previous reports, CT images of CAPNON typically showed solid calcifications, and MRI often revealed a well‐defined lesion that was uniformly hypointense on both T1‐ and T2‐weighted images without perilesional edema .…”

Multiple Calcifying Pseudoneoplasms of the Neuraxis

“…The radiographic appearance on CT is nonspecific and consistent with a well-demarcated and calcified intracranial mass. Consequently, CAPNONs are frequently confused with other intracranial lesions, including cavernous malformations, meningiomas, malignant lesions, and infections, such as tuberculosis [6-7]. The appearance of CAPNONs on MRI has been described as a hypointensity on T1- and T2-weighted images with minimal linear internal or partial rim of contrast enhancement [7].…”

“…However, the presence of all these elements in a single lesion is highly variable, and based on previous reports, lesions might not show all of these features [7]. Moreover, the mitotic activity and cellular atypia of the palisading cells is typically minimal or absent [6], and immunohistochemical stains are positive for vimentin and epithelial membrane antigen (EMA) and negative for S-100 protein and glial fibrillary acidic protein (GFAP) [2]. The EMA reactivity may support an arachnoid cell origin, but the tissue of origin in CAPNONs is still in question.…”

“…It has been proposed that these tumors may arise from a reactive proliferative process [3], a metaplastic transformation [4], or a neoplastic development [5]. Since the microscopic features of CAPNONs were first described in 1978, only 40 intracranial lesions have been reported in the literature [6]. In all instances, intracranial CAPNONs have been found as a solitary mass and have been associated with nonspecific imaging findings suggestive of a well-circumscribed, densely calcified lesion.…”