A 36-year-old female presented with cerebral infarction due to severe vessel stenosis after spontaneous rupture of a craniopharyngioma, manifesting as aphasia and drowsiness. Neuroimaging showed the suprasellar cystic tumor with wall enhancement and cerebral infarction in the left temporoparietal region, and also enhancement of the left sylvian fissure and prepontine cistern. Angiography showed se vere narrowing at the C₁ portion of the left internal carotid artery (ICA) and the M₁ portion of the left middle cerebral artery (MCA). The tumor was subtotally removed via a bifrontal craniotomy. There was accumulated milky-white debris around the left ICA and MCA. She became alert within a few days postoperatively.Repeat angiography 1 month after surgery demonstrated slight improvement of vessel narrowing. The neuroimaging and intraoperative findings suggested that the stenosis was due to vasospasm induced by chemical meningitis resulting from cyst rupture.

Subarachnoid haemorrhage (SAH) often leads to subarachnoid fibrosis and resultant normal pressure hydrocephalus; however, how subarachnoid fibrosis occurs is unknown. We examined the changes within arachnoid granulations (AGs) and the subarachnoid space (SAS) chronologically at the parasagittal region obtained from patients with SAH at autopsy and made comparison with controls by immunostaining for cytokeratin, specific marker for leptomeningeal cells and by the elastica Masson-Goldner methods. Within a week some AGs were torn, and many inflammatory cells filled the AGs and SAS. Cytokeratin positive cells were scarce. During the next two weeks cytokeratin positive cells increased. After three weeks, AGs and SAS were filled by dense deposits of extracellular matrices surrounded by multiple layers of leptomeningeal cells.

Summary Pituitary tumours develop at a high frequency in p27-knockout mice and retinoblastoma gene-knockout mice, which suggests that cell cycle regulatory genes, such as cyclin-dependent kinase inhibitor genes, are involved in the tumorigenesis of pituitary adenoma. Analysis of p21 and p27 gene abnormalities in human pituitary adenoma was performed in 28 pituitary adenomas by polymerase chain reaction-single-strand conformational polymorphism. No point mutations were detected in these genes. As no abnormalities of the p21 and p27 genes were observed, and if these genes are indeed inactivated, it is likely to be via transcriptional or translational defects.

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