Meningeal Anaplastic Hemangiopericytoma

Case Report

Austin Oncol. 2016; 1(1): 1004.

Meningeal Anaplastic Hemangiopericytoma

de Julian Campayo M¹*, Gaona-Morales J², Broseta-Torres R² and De las Peñas R¹

¹Department of Neuro-Oncology, Consorcio Hospitalario Provincial de Castellon, Castellon, Spain

²Department of Neuro-Pathology, H General Universitario de Castellón, Castellón, Spain

*Corresponding author: María De Julian Campayo, Department of Neuro-Oncology, Consorcio Hospitalario Provincial de Castellon, Orphan and Rare Tumors Spanish Group (GETHI), Castellon, Spain

Received: December 10, 2015; Accepted: February 08, 2016; Published: February 10, 2016


Hemangiopericytoma (HPC) is a rare tumor with high risk of recurrence at neural and metastatic potential level. We report the case of a woman with a primary Meningeal Anaplastic Hemangiopericytoma (MHPC) at right temporal lobe. In the same way, given the low frequency of this tumor, we have reviewed the available data on its characteristics, as well as its therapeutic management.

Keywords: Hemangiopericytoma; Intracranial meningeal neoplasm

Case Presentation

The case features a 66 year old woman with a history of high blood pressure during pharmacological treatment. She had no other pathological history. She presented with a right hemicranial headache which had become resistant to regular analgesics. The physical exam, including neurological and eye fundus tests, showed no abnormalities.

The Computerized Tomography (CT) scan showed a right temporal lesion which was hyperdense, with hypodense centre and marked perilesional edema, compression of the right lateral and third ventricles, as well as subfalcine herniation with intense enhancement after administration of contrast. In the Magnetic Resonance Scan (MRI), we saw a lesion of 55x45x45mm, with deformity of the Silvian fissure. This was an isointense T1 lesion, with the central area being of less intensity, markedly heterogenous in T2 Flair and spin echo sequences, leaving the hyper intense central areas – which describe a variegated morphology – visible. This coincided with the areas of greater magnetic susceptibility in T2 sequences, attributable to the presence of necrosis and vascular structures. In the periphery of the lesion, we could see a displacement of the vessels, with no signs of infiltration. This was surrounded by a digit form vasogenic edema, which causes displacement of the parenchymatous structures of the basal ganglions and of the middle line, with the ipsilateral ventricle being collapsed. After the intravenous administration of gadolinium, the lesion was intensely enhanced, leaving a non-captant central area, with no clear “dural tail”, although it appeared to be in contact with the lesion at its posterior part (Figure 1). The perfusion sequence reveal great lesion vascularization, with a CBV always greater than x4, at some points even reaching x12. Spectroscopy didn’t offer any specific defining characteristics.