The first transcranial surgery of the pituitary tumor was performed by Horsley V in 1889. In 1907 Scholoffer H succeeded in the transsphenoidal surgery (TSS) for a pituitary tumor of an acromegalic patient via the superior nasal approach. The prototype of TSS has been established by Cushing H (sublabial & submucosal approach) and Hirsh O(endonasal & submucosal approach) in 1910.Then, in 1960’s Hardy J had developed TSS using X-ray fluoroscopy and surgical microscope. Since then, with the rapid progress of endocrinology and imaging diagnoses such as CT scan and MRI, TSS has grown and flourished for several decades. In 1990s the endoscope has been introduced to TSS and has rapidly spread in terms of its wider and clearer operative view. Now the endoscopic TSS has been used not only for the pituitary surgery, but also the midline skull base surgery.

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Subependymal giant cell astrocytoma (SEGA) is the most common central nervous system tumor in patients with tuberous sclerosis complex (TSC). Although SEGA is a generally benign tumor (WHO grade Ⅰ), it gives rise to focal neurological deficit and obstructive hydrocephalus. At this point, surgical removal is the standard treatment of SEGA. But not all SEGA could be safely and completely resectable. Gamma knife radiosurgery is another option for the primary or adjuvant treatment for SEGA. Because of highly variable response and possibility of adverse effect, we need larger patient populations and longer follow-up study. Recently, mTOR inhibitor has been approved as a safe and efficacious molecular targeted drug for the treatment of SEGAs. However, SEGA can recur a few months after drug discontinuation. Long-term efficacy and safety of mTOR inhibitors should be evaluated with future studies.

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Rathke cleft cysts (RCCs) are benign cystic lesions of the sella that arise from remnants of the embryonic Rathke residual pouch. RCCs are common incidental findings in 4-33% of autopsy cases and on imaging, and most remain asymptomatic. However, RCCs can become sufficiently large and rupture to cause severe headache, visual field defects and hypothalamic pituitary dysfunctions. Asymptomatic RCCs are typically followed by serial imaging, while symptomatic RCCs are managed by surgical decompression. Although a headache and the visual disturbance are improved by surgical treatment, the pituitary insufficiency is not often improved. It is thought that an irreversible disorder due to the local chronic inflammation involves the pituitary gland. MRI reveals well-demarcated homogenous lesions with variable intensity that is highly dependent on the protein concentration of cyst contents, which can range from clear, CSF-like fluid to thick, mucoid material. Rates of recurrence after surgical treatment range from 11 to 18 % in large series, and higher rates of recurrence are associated with inflammation and reactive squamous metaplasia in the cyst wall. As the natural history of RCCs remains unclear and the mechanism of progression of these cysts is not understood, it might be difficult to determine when we should do the intervention of the surgery.

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Glioblastoma cells release and exploit glutamate for proliferation and migration by autocrine or paracrine loops through Ca²⁺ -permeable・-amino-3-hydroxy-5-methyl-4-isoxazolepropionate -type glutamate receptors (CP-AMPAR). Here we show the molecular mechanism behind glioblastoma cells expressing CP-AMPAR, and refer to its role for gliomagenesis.

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