An 81-year-old female presented with a giant aneurysm of the distal anterior cerebral artery (A 3 ) which grew from a small saccular aneurysm to a huge aneurysm within 36 months before manifesting as a mass lesion. The thrombosed portion of the aneurysm showed growth, whereas the aneurysmal cavity did not change in size. Computed tomography and magnetic resonance imaging showed new bleeding in the thrombosed portion. Hemorrhage into the thrombus and/or aneurysmal wall might have caused the aneurysmal growth. She refused surgery and was discharged with no deficits. Distal anterior cerebral artery aneurysm which shows neuroimaging signs of growth requires regular follow up as such lesions may become giant before manifesting clinical symptoms.

BACKGROUND The purpose of this study is to indicate that oxidative stress may contribute to occurrence of meningiomas. Recently, it was reported that aside from the neurofibromatosis type 2 (NF2) gene mutations, the calpain‐dependent proteolysis of the NF2 gene product, merlin might be closely related to the development of certain NF2‐related tumors. Although meningiomas are well known to occur more frequently in aged persons, it still remains unknown why calpain activation occurs predominantly in them. Because the production of free radicals with aging might be one of the causes of calpain activation especially in leptomeningeal cells being devoid of blood supply, the authors examined the relations between μ‐calpain activation and merlin proteolysis induced by the oxidative stress. METHODS The authors examined 12 patient‐derived sporadic meningiomas and their primary cultured cells. Malignant glioma cell line (U‐251MG), which had no relation to NF2, was used as a control. They were exposed to hydrogen peroxide (H2O2) for 1 hour. After oxidative stress, they were examined by Western blot and immunofluorescence microscopic analyses. RESULTS Despite the consistent expressions of activated μ‐calpain in 11 of 12 meningioma tissues, this calpain activation completely disappeared after culture; instead the full‐length merlin appeared again in 8 of 11 cases. The treatment of cultured cells with hydrogen peroxide induced both μ‐calpain–dependent cleavage of merlin and reduction of an intrinsic calpain inhibitor calpastatin. Such proteolysis was significantly blocked by a specific calpain inhibitor, Z‐LLal. The full‐length merlin was immunocytochemically colocalized with activated μ‐calpain at the plasma membrane, and, after μ‐calpain activation, the fragment of merlin translocated to the perinuclear cytoplasm or into the nucleus. CONCLUSIONS These findings suggest that oxidative stress‐induced activation of μ‐calpain causes proteolysis of merlin conceivably to impair cell adhesion and/or contact inhibition of meningioma cells. Cancer 2001;92:2662–72. © 2001 American Cancer Society.

A 65-year-old male who had previously received curative treatment for a pineal tumor presented with an extremely rare case of primary central nervous system (CNS) primitive neuroectodermal tumor (PNET) of the spinal cord manifesting as progressive tetraparesis. Although the histology was not verified, highly radiosensitive tumor was suspected because of the benign clinical course for over 20 years after only radiation therapy. Magnetic resonance imaging demonstrated an intramedullary tumor extending from C5 to T1. He underwent partial resection and histological examination revealed blue tumor with undifferentiated small round cells. Immunohistochemically, c-kit was negative but CD99 was strongly and diffusely positive. Therefore, rearrangement of the Ewing sarcoma gene was examined to determine the presence of peripheral type of PNET. The results were negative and systemic workup revealed no other disease. These findings led to the diagnosis of primary intramedullary CNS PNET of the spinal cord, and suggested that the spinal cord tumor occurred independently of the prior pineal disease. The residual tumor was controlled by postoperative local radiation therapy.

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The authors report an extremely rare case of de novo spinal teratoma after treatment for intracranial germ cell tumor. A 17-year-old male developed pain of bilateral lower extremities and urinary retention 18 months after complete remission of intracranial mixed germ cell tumor. Magnetic resonance imaging revealed a huge spinal tumor associated with spina bifida occulta. Total resection was performed, and histogenetical findings led to the diagnosis of a mature teratoma with normal p16 gene, whereas analysis of intracranial tumor showed p16 deletion. The spinal anomaly and genetic analysis strongly suggest that the spinal teratoma was a de novo tumor rather than a metastasis or dissemination of the original intracranial germ cell tumor.