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A 26-year-old male with large intraventricular meningioma developed acute hydrocephalus postoperatively, which was difficult to manage. After a repeated course of dilated and slit-like ventricle, he gradually presented a disturbance of consciousness, which was recovered by the use of bromocriptine, suggesting akinetic mutism. At the chronic stage, he suffered from symptoms of hydrocephalus again. Time-slip MRI revealed the stasis of CSF flow around the third ventricle. Neuroendoscopy disclosed that the foramen of Monro was occluded with membrane. After endoscopic third ventriculostomy as well as penetration of the foramen, the symptoms disappeared and hydrocephalus was resolved. This is a rare case of akinetic mutism after complicated management of hydrocephalus associated with intraventricular meningioma.

We review 48 cases of meningioma treated with Gamma Knife radiosurgery. The mean marginal dose was 15 Gy and the mean follow-up was 12 months. Follow-up computed tomography and magnetic resonance imaging showed tumor shrinkage in 19 cases, central necrosis in 1 case, loss of contrast enhancement in 1 case, and no change in 27 cases. We noted 4 cases of radiation-induced edema in supratentorial meningiomas.

Many factors have been suggested as possible mechanisms for the development of peritumoural oedema in meningioma. Venous compression by the tumor is thought to be one factor, but reports presenting a direct relationship between venous compression and the formation of oedema are rare. We have recently observed 6 meningioma patients in whom venous stasis contributed to peritumoural oedema. The stasis was due to 1) compression of an adjacent cortical vein by the tumour with stasis at the site of compression and/or its distal portion, 2) compression of adjacent brain by the tumour with prolonged perfusion and delayed venous return (visualized as pial staining in the capillary and venous phases), and 3) presence of an early draining vein linked to a nearby cortical vein with stasis at its periphery. Venous compression and stasis seem to be related not only to the formation of peritumoral oedema but also to the occurrence of haemorrhagic infarction after the resection of meningiomas.

The signal intensity of magnetic resonance imaging (MRI) was compared with the histologic findings in 20 cases of neurinoma and 18 cases of meningioma. The apparatus was a Hitachi G-10 unit (0.15 T). The pulse sequences were SR (500/32), SE (1200/60), IR (1400/400). The intensity of tumor signal, as compared with that of normal white matter signal, was divided into 9 grades. In neurinomas, the signal intensity appeared markedly low with IR and markedly high with SE sequence in the Antoni B type, while it was slightly low with IR and minimally to markedly high with SE sequence in the Antoni A type, and intermediate between Antoni A type and B type in the mixed type. In meningiomas, it appeared moderately to slightly low with IR and slightly to moderately high with SE sequence in the meningotheliomatous type, minimally low with IR and minimally to slightly high with SE sequence in the fibrous type, and intermediate as compared with the above two in the transitional type. The angiomatous type was characterized by a low intensity on SR and IR images and an iso to high intensity on SE images, while the psammomatous type showed a low intensity with all of the sequences used. We clarified that the signal intensity on MRI varied among different histologic types of neurinoma or meningioma, and correlated differences in the intensity of signals on MRI to that of histologic characteristics, such as size and shape of cells, intercellular material, intracellular biologic polymers, area of membrane surface, blood flow and calcified matter.