IS Case 601: Meningioangiomatosis

Alena Levit, MD

Imaging Sciences URMC

Imaging Sciences URMC 2010
Publication Date: 2011-11-17


The patient is a 44-year-old female presenting with seizures and migraine headaches


The patient is a 44-year-old female presenting with seizures and migraine headaches




Meningioangiomatosis (MA) is a rare, benign, hamartomatous cortical/leptomeningeal malformation. Histopathologic examination demonstrates cortical meningovascular proliferation with calcifications. MA lesions are typically solitary but may be multiple; diffuse lesions are very rare. MA often extends into cortex via perivascular spaces and it has no malignant degeneration.

MA is usually found in children and young adults and is more predominant in males. Other neurological abnormalities may be associated with MA, and include neurofibromatosis (particularly NF2) which is found in one-half of patients, meningioma, oligodendroglioma, arteriovenous malformation, encephalocele, and meningeal hemangiopericytoma. Majority of patients with MA typically present with intractable seizures and headaches, however MA can also be an incidental finding.

The accurate diagnosis of MA is important since MA is a benign, surgically correctable cause of seizures. The best imaging tools are MRI and CT. The best diagnostic clue on imaging is a cortical mass with calcifications. MA lesions are usually found at the cortex of frontal and temporal lobes, they are more predominant on the right than left. Rarely, MA may be found in the third ventricle, thalami, brainstem, and cerebellum.

The imaging findings for MA correlate well with the histopathologic features. Calcifications in the leptomeninges and perivascular spaces are best demonstrated on unenhanced CT. Calcifications may be either linear, granular, or gyriform in nature. Occasionally hemorrhage and cysts may be seen as well. There is usually no mass effect. MA lesions have homogenous enhancement on CT.

On MR T1WI, MA lesions are isointense with areas of signal void due to calcifications and with areas of hypointensity due to cystic components of MA lesions. On T2WI, MA is hyperintense with areas of signal void, appearing as target-like lesions with central hyperintensity. Cystic components of MA lesions appear hyperintense on T2WI. MA is slightly hyperintense with areas of signal void on PDWI. T2-GRE may be used to accentuate calcifications. MA has a homogeneous enhancement on contrast-enhanced T1WI.


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