Investigation of collapse.
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A solitary extra axial mass with a broad dural base at the junction of the right parieto-occipital lobes posteriorly is demonstrated. A thin CSF cleft is difficult to appreciate however is most conspicuous along the anterior aspect of the lesion with impression of cortical buckling. The lesion is predominantly isointense to adjacent brain parenchyma on T1, heterogeneous on T2 with several foci of intralesional gradient susceptibility artefacts representing blood products or calcium.
The lesion is vividly relatively homogeneously enhancing with a small dural tail. Diffusion restriction within the periphery and inferior aspects of the lesion. Extensive T2 signal hyper intensity involves the posterior frontal, superior parietal and posterior temporal lobes in keeping with vasogenic edema.
Associated focal mass effect with sulcal effacement and effacement of the posterior horn and trigone of the right lateral ventricle.
No midline shift. No transtentorial or transforaminal herniation. No overlying hyperostosis identified.
Moderately extensive periventricular and deep subcortical white matter FLAIR/T2 signal hyper intensity is consistent with microvascular ischemia.
The intracranial flow voids are preserved.
Solitary vividly enhancing extra-axial mass with a broad dural base is most likely in keeping with a meningioma.
The patient went on to have surgery.
MICROSCOPIC DESCRIPTION: The sections show a moderately cellular meningioma with attached dura. The tumor comprises whorls and nests with psammoma bodies. The tumor cells have ovoid nuclei but with no nuclear pleomorphism. Mitoses are inconspicuous. There is no tumor cell necrosis. Many blood vessels are present in the background and they have prominently hyalinised walls. Microcystic change is noted. Brain parenchyma is included in the biopsy and there is no evidence of brain invasion. No atypical or malignant change is identified.
FINAL DIAGNOSIS: Angiomatous meningioma (WHO Grade I).