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Loss of MSH6 occurred during the progression from an atypical prolactinoma to a pituitary carcinoma, which may have caused resistance to TMZ treatment. This case suggests that preserving MSH6 function is essential for responsiveness to TMZ treatment in MGMT-negative and p53-mutated atypical pituitary adenoma or pituitary carcinoma.

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C o r r e l a t i o n B e t w e e n M I B -1 S t a i n i n g I n d e x a n d t h e I m m u n o r e a c t i v i t y o f p 5 3 P r o t e i n i nR e c u r r e n t a n d N o n -r e c u r r e n t M e n i n g i o m a s Wild type p53 protein has been shown by recent investigations to be involved in the negative regulation of cell proliferation, whereas aberrant p53 protein has lost this negative regulation of cell growth. Wild type pS3 protein, which has a very short half-life, has generally been considered to be undetectable using immunohistochemical methods; however, according to a recent report, wild type p53 protein may accumulate in the nuclei because of a defective ubiquitin pathway. Aberrant pS3 protein has a longer half-life, and thus is visible using immunohistochemical methods. In this study, both the proliferative potential represented by the MIB-1 staining index (SI) and the immunoreactivity of pS3 protein in 51 intracranial meningiomas were studied applying immunohistochemical staining methods to archival paraffin sections.Recurrence of meningiomas is considered to be affected by a variety of clinical, biologic, and histopathologic factors, including the patient's age, sex, tumor location, extent of surgical removal, histopathologic findings, estrogen and progesterone receptors, and receptors for other growth factors. Among these factors, the proliferative potential of meningioma is considered by several investigators to be one of the most important. 1 "" In a previous report, we used an anti-Ki-67 monoclonal antibody, MIB-1, that can detect all proliferative cells in routinely processed paraffin sections, 3,612 and have shown that there is a statistically significant correlation between the MIB-1 staining index (SI) and recurrence of meningi-

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A 58-year-old woman and a 71-year-old woman presented with extremely rare skull base metastases from follicular thyroid carcinoma (FTC). Surgical removal and external radiotherapy were performed followed by iodine-131 ( 131 I) brachytherapy and thyroid hormone administration. The metastatic tumors in the skull base were well controlled. Treatment for skull base metastasis from FTC includes surgical debulking of the metastatic lesion, as well as complete resection of the thyroid gland, followed by internal irradiation with 131 I, external irradiation, and administration of thyroid hormone to prevent tumor growth by suppression of endogenous thyroid-stimulating hormone. Skull base metastases may be the initial clinical presentation of FTC, with silent primary sites. The possibility of skull base metastasis from FTC should be considered in patients with clinical symptoms of cranial nerve dysfunction and radiological findings of bone destruction.

A 34-year-old female presented with spontaneous intracranial hypotension (SIH) manifesting as severe postural headache and meningism. Magnetic resonance (MR) imaging with gadolinium showed diffuse pachymeningeal enhancement. She developed bilateral chronic subdural hematomas 4 weeks after the onset of the symptoms. MR imaging showed descent of the midline structures of the brain. The bilateral chronic subdural hematomas were surgically drained, with no remarkable pressure. Postoperative MR imaging showed complete resolution of the pachymeningeal enhancement and relevation of the midline structures of the brain. SIH is an uncommon and probably unrecognized condition because of the usually benign course. However, this case emphasizes that SIH is not entirely benign. SIH should be considered if there is no identifiable risk for intracranial hemorrhage, particularly in young patients. Neurosurgical intervention for the treatment of the underlying cerebrospinal fluid leak may be required if SIH persists.