The thermal damage threshold of normal brain tissue was evaluated from immediate and delayed histological changes caused by hyperthermia treatment of normal monkey (Macaca fuscata) brains. A 2450 MHz microwave antenna and an antenna cooling system devised by our group were used for in terstitial hyperthermia treatment. The antenna within the cooling system was inserted through a small craniectomy under general anesthesia. The temperature at a reference point, 4 mm radially away from the surface of the cooling system, was maintained at 42, 43, 44, 45, or 46°C for 60 minutes. Eighteen animals were treated and sacrificed immediately after the treatment, while nine animals were treated and sacrificed 7 days after the treatment. The histological changes were studied microscopically on sec tions stained with HE or Kluver-Barrera's method. The non-survival experiment demonstrated that areas heated at 44°C or below showed no obvious irreversible changes. The survival experiment showed areas heated at 44°C or above developed coagulative necrosis. These histological findings in dicate that thermal damage occurs in normal brain tissue after heating at 44°C or above for 60 minutes, suggesting that the safety limit for brain hyperthermia is 43°C for 60 minutes.

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An immunohistochemical study of glial fibrillary acidic protein (GFAP), S-100 protein, cytokeratin (CKER), epithelial membrane antigen (EMA), and transthyretin (TTR) was carried out on 11 cases of choroid plexus papilloma (CPP) and 19 of ependymoma, using the peroxidase antiperoxidase technique. Among the 11 cases of CPP, all 11 were positive for CKER, EMA, and TTR, 10 for S-100 protein, and five for GFAP. Most of the GFAP-positive papilloma cells were simultaneously positive for CKER. However, these GFAP-positive cells were negative for TTR. Among the 19 cases of ependymoma, 16 were positive for GFAP, 17 for S-100 protein, three for CKER, eight for EMA, but none for TTR. Some GFAP-positive cells were also stained for CKER. However, TTR was not found in any of the ependymal cells. These findings suggested that CPP cells which show ependymal or glial differentiation lost the ability to synthesize TTR which is known to be synthesized in the epithelial cells of the choroid plexus. The more GFAP-positive cells present in a CPP, fewer TTR-positive cells are present. Though CPPs are usually easily distinguishable from ependymomas, occasional doubt arises concerning the differential diagnosis between CPP and papillary ependymoma. TTR can be a very useful diagnostic marker of CPP.